Day 1: Palm Springs to some point 91 miles into the CA desert. The first day of my four day ride is dedicated to my Dad and everyone else who has had the terrible experience of Alzheimer's disease. I had a great start to the ride as a group of the previous day’s riders saw me off from the Palm Springs hotel. Quite a scenic ride, skirting just north of Joshua tree National Park, by 29 palms, then into the desert, no houses, very few cars, very quiet and starkly beautiful. The only detraction was the 110 degree heat and some nasty hot headwinds. Water bottles warmed up to very hot tea temp in about 10 minutes, my fingers felt like they were burning from the reflected heat from the pavement, which is possibly why no one lives there…perhaps not the best day to ride 90+ miles. As exhausting and hot as this day was, I kept thinking (as much as it is possible to think in the heat) that anyone suffering from AD would trade places in an instant. Certainly I could make it through 90 miles if they can make it through one day with AD. I had a great support crew (Melanie and Evan) and had cold water, caring people and good company whenever i needed it, and at the end of the day, a drive back to 29 Palms with a nice dinner and cold hotel room.
Day 2: Middle of the CA desert to Parker, AZ (70 something miles) The second day is dedicated to my Mom and everyone else who has served as the primary caretaker for someone with AD. The second day we drove back to where we stopped the previous evening, and started off in slightly cooler morning temps. Another long, hot day, some wicked cross winds along a two lane road without any shoulder and a fair number of trucks heading toward Parker/Lake Havasu. Certainly gave Melanie (my car escort) and I a fair number of grey hairs. But again i kept thinking that any primary caretaker would trade places with me in a heartbeat, at least there was an end to the skinny highway (a beautiful end at the Colorado river which was a gorgeous, clear turqouise), another good dinner, a cool hotel room and the hope for a cooler day tomorrow.
Day 3: Parker, AZ to WIckenburg, AZ (80 something miles) Today is semi-selfishly dedicated to all the Alzheimer's researchers who have dedicated their lives to trying to find an answer to this awful disease. A treat in the morning cloud cover: no wind and relatively cool temps. Actually drove out to Bouse, AZ to start riding there. We paid for the dirty trick; strong wind picked up from the south east, which of course was directly where we were heading, so what I was hoping was finally going to be an easy day started out as a struggle. We rode past a Hollywood movie set in the middle of nowhere, apparently filming Fast and Furious 5. They were just cleaning up the site, apparently a train wreck, and were loading 5 or 6 very expensive sports cars onto a trailer. I was struck by the thought that the single trailer could fund several Alzheimer’s disease research labs for many years, but instead was just a scene in a movie. By afternoon, the wind and us both changed directions, so it was a relatively pleasant afternoon, even with the sun. Went by a flea market of sorts that came up out of seemingly nowhere and disappeared quickly into nothing—we all wondered if it was a mirage. Last 10 miles was a wonderful downhill coast into Wickenburg which is really a pretty quaint town. The cooler day overall was a very welcome and needed change.
Day 4: Wickenburg, AZ to Phoenix, AZ Our last day, relatively short, and dedicated to everyone who has helped contribute to Alzheimer research. The ride out of Wickenburg was cloudy, cool (by previous standards), beautiful, downhill with big shoulders. This is what bike touring should be like! It was a bit of a shock to hit the outskirts of Phoenix, (appropriately called Surprise), back to malls, gas stations, road construction. But it was good to be done and heading home for a good rest. Thanks to everyone who has contributed to this effort, but especially thanks to Mel and Evan for making what could have been an unbearably hot long four days into an almost too short very fun tour. Good luck to Matt who will have a long, long climb tomorrow!
-Michael Sierks, Ph.D. Dr. Sierks is a Full Professor in the Chemical Engineering Department at Arizona State University in Tempe. Dr. Sierks became interested in Alzheimer’s after his father and aunt were diagnosed with the disease. His research focuses on developing better tools to help study the complexities involved in protein misfolding diseases such as Alzheimer’s and Parkinson’s diseases.
The miles traveled over our first two days seemed to create a special type of gravity which pulls one farther under covers, and into a bed. Luckily this was easy enough to overcome by the thought of this being our final leg towards Los Angeles, and easier still because we would have a fresh pair of legs joining us: those of Harry Johns, the CEO of the Alzheimer's Association. I looked forward to conversing with him about the state of AD research, care and public policy, and I was not disappointed.
After we found a stretch of quiet roads a few miles out of Ventura, we got to talk about my research and recent progress in the field. Harry followed along with the ease of a scientist, though he is not one. He shared with me that at the helm of the association, one gets to interact with the best of the best researchers and doctors, and with this immersive exposure he has picked up what seems to be enough knowledge to qualify for an advanced degree. Harry gets such a birds-eye view of the field that it was refreshing to hear his outlook. From the previous two segments I had learned for the first time about the research my fellow riders were working on back at UCLA, I had not yet had any interaction with their research group. That speaks to the breadth of neuroscience research at UCLA even within the Alzheimer's field, as well as to the narrow focus that each of us falls into in our own work. More than once it struck us that the Breakthrough Ride was benefiting the researchers participating: in addition to driving our message to the public, the ride is helping to create bridges between research groups working toward a common goal.
The ocean breeze and vistas reminded us that we were fortunate to ride along the CA coast into LA, and eventually we came upon familiar territory, reaching sections of the Pacific Coast Highway that we had cycled on during our training rides. Our route took us east at Santa Monica towards Brentwood and Westwood, literally passing in front of my apartment, but onwards we rode towards the signing event we knew was waiting for us in front of the Kodak Theater. We were treated to a scenic ride through Beverly Hills, though we noticed the traffic becoming more congested, and drivers sometimes irritated to have cyclists in their lanes. Though I have been living in LA for almost a year (from the time I began a postdoc at UCLA), we rode through areas I've never seen and we had to keep a very close eye on our cue sheet, leading us left and right, left and right, weaving our way to Hollywood and Highland; we needed direction in our own city. Looking back, I'm realizing its not unlike the Alzheimer's community: we need a map, a route, a plan, as to how we can best attack this disease. A plan for research looking at the disease from many angles, a plan for funding and public policy, and a plan for patient care until we can actually treat this disease. With the passage of the Breakthrough Act, the Alzheimer's field can have the overarching plan it desperately needs.
We wouldn't have had such an easy time reaching the Kodak Theater without our directions laid out, and it was all worth it when we did. The crowd who had gathered burst into cheers the moment they saw us turn the corner, and gave us an amazing welcome. I wondered if they really understood what it was like to have been on the bicycle for a total of about 18 hours over the past three days, but each one was so appreciative of our efforts, it didn't matter. They thanked us for participating in the ride, for bringing attention to the cause, and for the research we do each and every day. For me that was special, because in the lab with our instruments and experiments, it's easy to lose sight of why we do this. I see proteins not patients in my work, so their "thank you" meant a lot.
-Eric Y. Hayden, Ph.D. Postdoctoral Scholar, Neurology David Geffen School of Medicine University of California at Los Angeles
Day 2, we rode from Lompoc to Ventura-94 miles, total.
Lompoc California is home to Vanderburg Air Force Base, where some of the great achievements of American science are shot into space or return from it.For our 7:00 AM takeoff,it was a cold mistymorning and this time we had two new riders in Greg Cole and Ed Teng.The beginning was a long, 19-mile stretch of climbing, although not too steep.While riding, Greg and Edswapped insights from their experience at the Alzheimer's Association International Conference on Alzheimer’s Disease (AAICAD) in Hawaii earlier this July.They also learned about Eric’s line of research in the Teplow lab, purifying and characterizingunique species of beta-amyloid oligomers, and the different types of Alzheimer’s toxins.After taking a short stretch off to nurse an injury, Karen joined us at the top of the hill and was pleased to find out that with a little ibuprofen and a lot more pedaling, she was able to work out the pain in her joints.At the end we were trying to figure how much exercise is good for your brain and might reduce your risk for Alzheimer’s, and how much is too much.
We took a few wrong turns and went up some additional hills, much to everyone’s chagrin, since the rest of the trip was supposed to be relatively flat.With few other options, we toughed out a few stretches on the 101 freeway breathing the fumes of cars and trucks, but off on the right we could see the Pacific Ocean dotted with oil platforms, reminding us of trouble in the Gulf.We then were delighted to turn off on to a long series of isolated, scenic and safebike paths either wooded or right along the water,until we got to the hotel.Half way through Ed Teng lost his energy and almost gave up. Somehow though, he found a second wind and led the pack at the end, perhaps because Greg Cole took a series of phone calls about troubleshooting Western blots for Alzheimer’s biomarkers from the lab.
We are so glad to have the ride down the coast of California with its marine layer and fog,and wish the future riders riding across the country and the deserts and heartland, a safe journey, drinking their electrolytes before they are thirsty.We launched this morning where rockets took off and ended upon America’s edge. Now American Science needs to conquer one of the biggest problems on earth, Alzheimer’s disease.We are proud to be part of the team taking on this challenge.
Sally Frautschy , Eric Hayden, Karen Gylys, Ed Teng and Greg Cole are the UCLA Mindsavers
It's Not Too Late To Sign The Petition To Make Alzheimer's A National Priority...When? "Now!" said our President and CEO of the California Southland Chapter, Bettina Kurowski, in her speech on Thursday, July 22 as we applauded 5 riders that came riding into town from San Luis Obispo to join us in Los Angeles at Hollywood Blvd. and Highland while we rallied a crowd of people from all walks of life to sign our petition.
Congratulations to the riders from UCLA Research Team who traded their lab coats in for bicycle shorts and jumped on bikes to ride for the cause: Sally, Greg, Edmund, Karyn, and Eric. Joining this remarkable team of UCLA cycling researchers, was our very own President/CEO of the National Alzheimer's Association, Mr. Harry Johns who cycled his way into Los Angeles. As Mr. Johns addressed the crowd, he warned us that if we don't change the course of Alzheimer's, "it will cost Americans trillions of dollars, yes a trillion with a T," in care, treatment, and services. Congress has failed to act over the years; therefore we must ACT, and NOW, to change the course of Alzheimer's by signing the petition to make Alzheimer's a national priority.
Let's also wish all the riders well as they travel the country, visiting more than 65 congressional districts and countless towns and cities.
The time to ACT is NOW...as many as 5.3 million Americans have Alzheimer's disease. In addition, we were reminded about those living with Early Onset Alzheimer's, as the dynamic duo Susan Franklin and her husband Serge (members of our Early Stage Memory Club) shared their personal story about Susan's early onset diagnosis and their challenges.
We need your help as these dedicated cyclists make this historic cross-country journey to Capitol Hill to gather 50,000 signatures, arriving at Capitol Hill on World Azheimer's Day, September 21, 2010. Sign the petition today and become a part of tomorrow's solution. I am excited and proud to be a part of the Alzheimer's Association Ambassador Team fighting for A world without Alzheimer's disease.
In Health, Bryan F. Gaines Education and Outreach Coordinator, Alzheimer's Association California Southland Chapter Alzheimer's Ambassador 35th District, Congresswoman Maxine Waters
For the first day of our ride it would be myself (Sally Frautschy), associate professor Karen Gylys, and postdoctoral fellow Eric Hayden, all of us from UCLA. At 6:00 a.m., we were debriefed on our mystery route, as if we were in the CIA. When we started out at 7:00 a.m., it was drizzling and cold and the Alzheimer Breakthrough RV “Pony” support vehicle extraordinaire was out of commission. We found out later in the day that the repair shop staff stayed up all night to fix the RV for us so we could have it for the 2nd day of our journey. Originally the riding was fast and flat and without wind, making us feel extremely guilty since our breakfast with the Stanford group completing the previous leg (Tony Wyss-Coray and Phillip Jaegger) revealed that they rode 70-90 miles a day fit and fast with temperature fluctuations from 55 degrees to 110 degrees.
Thus we were slightly relieved to see a steep hill, but then we each had a bicycle incident. First two semi-trucks going opposite directions on a fairly narrow road with no shoulder were passing at the same time when my water bottle cage lost a screw and fell into my leg causing me to fall toward the middle of the road. The trucker yelled at me because he had to stop, but miraculously no one got hurt. Then Karen’s chain fell off, which was easy enough to fix, and shortly thereafter Eric Hayden, worrying about Karen and I, looked ahead toward us and away from the road and his tire slipped over the narrow paved road onto the abruptly lower dirt shoulder at 20 MPH, and he scraped up his knee. Luckily, it wasn't serious and he recovered without a problem.
In addition to the huge fields of crops that we were cycling through, we got to see lots of wildlife. I almost ran over a diamond back rattlesnake sunning itself on the pavement. We saw an egret pass the road, a red-tailed hawk, and a mouse running across the road in the midst of broccoli stems that had fallen off the produce trucks.
Passing through Vandenburg Air Force base, a nice elderly lady stopped her car and asked, "Am I lost?" She was looking for the entrance to the base. She was very concerned, and we didn't know the area all that well since we were just passing through. We helped her find the directions to the base by asking the nearby workers in the field. She introduced us to her sweet Yorkshire terrier named “baby” whom she was clutching tightly to keep her calm. She reminds us why we are on this ride.
It felt good for all of us to wear the Breakthrough Ride jersey, it really seemed like we were a team working towards something bigger than any of us. We are excited to be joined tomorrow by Greg Cole and Ed Teng, whom we work with at UCLA. Especially because we hear that from Lompoc to Ventura it will be a 90 mile ride!
The third segment of our relay leg was leading Tony, Eric, and I from the small agricultural town of King City to San Luis Obispo, a ride of around 72 miles.
Third days are special days: Everyone gets out of bed a little slower than before; every bone aches a little more than yesterday; and that persistent morning fog feels just a little cooler than the damp starts we had on the days one and two. I guess the cumulative effects of around 15hrs saddle-time started to show and it seemed that we all had gotten some lead weights tied to our feet when we wobbled over to Denny's for our early morning eggs, coffee, and ibuprofen. Despite the initial lack of momentum we decided to quickly get moving after Melanie and Evan revealed our route for the day and - more importantly - the accompanying route profile. Some 20 miles into the ride the profile quickly climbed from 200ft to a 1500ft pass in less than 3 miles. Ouch! That would be a spot you really want to hit before the sun comes out and bakes you. So off we went at 6.50am to make our way out of the Salinas Valley and up into the hills of Fort Hunter Liggett. Luckily most of the pain in our legs and rear-ends subsided after the first 10 miles, or maybe our bodies just got used to it ...
The vegetable fields that were so prevalent yesterday slowly turned into rolling California grassland and then into oak-covered hills as we approached the Santa Lucia Range. The golden grasslands were covered with early morning mist and the blue sky just started to peek through the banks of fog hovering over our heads as we hit the foothills. What a pristine country! We had to stop for a moment to inhale the beauty of this place.
Just as we were settling into a good cruising speed we realized that Melanie, our support van driver, had not passed us since breakfast, and we got a little worried about having taken a wrong turn somewhere in the carrot fields. After getting to a spot with cell phone coverage we got the shocking message: The Pony was hurt! But how bad was it? Were there any injuries to the crew? Would this be the end of the ride for all of us? To our great relief we soon found out that the Pony was only lame, did not have to be put down, and could possibly even recover in a day or two. And the crew was unharmed, too. As it turns out, the hydraulic pumps that operate the loading dock of the Pony had tucked themselves behind some silly pole at a gas station and decided to stay behind while Evan rode off into the morning fog. Thankfully we were blessed with incredible tour operators, and Mel and Evan quickly redistributed food, water, and supplies from the Pony into the support van. While Evan stayed behind to get the Pony's wounds welded, Melanie caught up with us and the rest of the day would progress without any further incidents.
We approached that dreadfully steep climbing section at around 9am as the sun had just burnt its way through the fog and the temperature quickly rose to the 80s with a strong upwards trend. We had to push on if we wanted to make it up and over that pass without a heat stroke. We filled our water bottles and attacked the incline one by one spaced out over a few minutes. Tony led the pack and made it to the top first. There he would stand and cheer at us, waiting to spray us with his water bottle as we approached. Then we flew down from the pass through 20 miles of rolling but slightly downhill grassland into the heart of Fort Hunter Liggett. Soon the only other vehicles on the road were Humvees roaring by and automatic rifle fire in the distance would occasionally interrupt the hum of our tires on the dead straight roads. Eric decided to do some office work in the supply van and so Tony and I set out to pass through the grassy hot-pot of the Hunter Liggett high basin by ourselves. We were approaching noon and the heat was quickly picking up. Staying hydrated was everyone's biggest concern and we went through two bike bottles every 30 min or so. Just before lunch break the temperature on my bike computer showed 109F and the hot air was blowing up from the asphalt, drying layers of salt onto our faces. Ice packs cooled our heads as we munched away on our sandwiches under a shady tree. The afternoon included a final climb out of the Hunter Liggett basin and then a long and hot decent back down to the Salinas River and Paso Robles. There our ride ended and we travelled the last few miles to San Luis Obispo in the comfort of the air-conditioned supply van along US-101.
After a long shower and some relaxation in the hot tub, we met up with the riders for the next segment: Sally Frautschy and Eric Hayden. We had many great stories to share with them over dinner and made sure that the spirit of the ride got passed on. What a remarkable three days!
Thank you to the organizers, the Alzheimer's Association, the petitioners, the donors, and everyone involved who made this event possible. And special thanks to our fantastic road crew: Melanie, Eric, Evan, Joey, and Celest. Go Breakthrough Riders, Go!
- Philipp Jaeger, MSc.
Philipp Jaeger is a graduate student in Tony Wyss-Coray's lab at Stanford University.
Tony Wyss-Coray, Ph.D., is an Associate Professor of Neurology at Stanford University and a Research Career Scientist at the Veterans Administration Palo Alto Health Care System.
The second day of the Breakthrough Ride was going to lead us from Santa Cruz to King City in the heart of Salinas Valley.
It was 5:25 am when the alarm went off and I had to pull my sore body out of bed. A hot shower helped a bit and I definitely felt better after a good breakfast at a Diner in Santa Cruz. My stack of pancakes was topped with a mountain of fresh strawberries and whipped cream and everybody seemed surprised that I managed to eat it all. But to be fair, we were just briefed that our ride today would be 99 miles!
The streets were still empty when we rolled out on this young Sunday morning and we were surprised to see the warm and sunny skies from yesterday afternoon replaced by coastal fog once again. Phil Jaeger came back from the wedding he attended last night for the ride ahead but Kurt and Bruce had left. Luckily, we were joined by our project manager Eric Goodwin, who, as we found out, coaches a cycling team in Chicago.
Off we went for day two, along the coast through Aptos, past Pajaro Dunes, and Watsonville. The scent of freshly turned soil merged into that of fresh cut cabbage and ripened strawberries – a tour de smell. At an intersection somewhere past Watsonville, we merged with a group of cyclers from the Monterey Velo Club and Eric was quick to advertise our ride. They were kind enough to let us ride in their draft to save some energy for the next five miles or so.
It had gotten warmer but there was still a layer of fog as we entered Salinas Valley, the birthplace of John Steinbeck. Around 10:30 the sun finally came out warming our muscles and producing an ever stronger tail wind up valley. There was no shade in this flat farming valley so we took refuge in the “Pony Cafe” for lunch. Ride staffers Melanie and Evan treated us with sandwiches and fruit and we even had iced coffees.
The wind was picking up and we were cruising behind Eric at an average speed of almost 20 mph over the next 40 miles on long agricultural roads. As we rode our steel horses (or carbon fiber…) into King City, tired from the strong wind and dusty roads, a huge tumble weed blew across the street just in front of us – what an amazing country. After a shower followed by a big steak, we were ready for bed.
Thank you to the whole Breakthrough Ride team for organizing such a breathtaking (pun intended) journey through the countryside. We are so privileged to be able to participate and I know this Ride will continue to inspire and sustain our dedication to research on Alzheimer’s disease.
And so it began...It was a cool (55 degrees) and foggy morning in San Francisco as myself (Bruce Lamb), Tony Wyss-Coray, Phillipp Jaeger and Kurt Lucin (all researchers at Stanford University) as well as Eric Goodwin (Manager of the Breakthrough Ride) gathered at 5:45 AM for our pre-ride breakfast. We were all nervous, excited and ready to get this ride going!
Upon arrival at the Marina Green Park Triangle, we saw the striking purple RV (nicknamed "The Pony") that will serve as our support vehicle for the entire ride across the country. Behind The Pony was the faint outline of the Golden Gate bridge that was shrouded in thick fog. We next met the Breakthrough Ride road crew, including manger, Joey, and staff Celeste, Evan and Melanie, the group that will support the ride all the way from Coast to Capital. In addition, we were joined by Harry Johns, the CEO of the Alzheimer's Association, who would be riding with us on this first day of the Breakthrough Ride. Upon receiving our daily briefing, we were ready to finally get underway!
After a brief ceremony, the countdown was on: 10, 9, 8, 7, 6, 5, 4, 3, 2, 1...GO! We jumped on our bikes and cautiously proceeded across the soft grassy knoll towards the road, as none of us wanted to fall in the first 50 yards of this trans-continental ride with cameras trained on our every move. It felt good to finally be riding and working towards our goal! I had attached the map of our route to my bike and was attempting to help direct us through the streets of San Francisco to get to Route 1, The Pacific Coast Highway. Despite my efforts we still had to back track from one wrong turn, but we were finally closing in on Route 1.
We reached the first major climb of the day. As we climbed, the fog became thicker and thicker, until finally visibility was reduced to less than a couple hundred feet. Our breathing became more labored and our hearts were now pounding. I called out to the other four team members, "Break!", and they answered "Through!", "Break!...Through!" "Break!...Through!" as we finally reached the top. It was a fun ride to the bottom, as Harry led the way, "pulling" the team along to the intersection with Route 1.
Soon after turning onto Route 1 (mile 15), we spotted The Pony sitting in a parking lot marking the first rest stop of the day. As we pulled in to the cheers of the road crew and support staff, we were all grateful to get some Gatorade, a snack, and a trip to the restroom. However, we were concerned about stopping too long, as the cool, damp weather was rapidly chilling our body temperatures. At this point, Harry Johns had to leave us for another engagement, but we continued on with the remaining four team members down Route 1 towards Half Moon Bay.
As we approached Half Moon Bay, the route took us to an all purpose trail that followed the shore. There were several creaky wooden bridges and beautiful blue and yellow wild flowers. While the fog by this point had partially lifted, we could still only imagine what the famous Northern California coastline looked like along the route. After a quick stop in Half Moon Bay and the departure of Phillip Jaeger, who was attending a wedding, Kurt, Tony and I continued on to our lunch stop at mile 45, which was at a beautiful beach along the shore. After a wonderful lunch of sandwiches, carrots, fruit and all the Gatorade you could drink we decided to continue on to the final push to Santa Cruz.
The last 35 miles of the day seemed a lot longer than the first 45, as our legs began to tire and our rear ends became increasingly sore. However, several events over this last stretch served as an inspiration and kept us working towards our goal. First, the fog finally cleared and we could now fully appreciate the breathtaking views as we passed along the jagged California coastline, although one had to be careful to keep your eyes on the road ahead! Second, a bicyclist approached us as we neared the top of a ridge and slowed to talk with us. "Hey," he said, "you are the guys riding for Alzheimer's disease, you're awesome. I read about you on Facebook!" Third, as we neared the final scheduled rest stop, we could see the purple Pony in the distance, but noticed a great commotion around the RV. As we got closer, we realized that the commotion was in fact the entire road crew dancing around the Pony in synchrony to their own silent soundtrack. We couldn't help but start to "hear" the same soundtrack and bounced along on our bikes for the last few miles of the day. Finally, we reflected on all of the incredible messages of support on the Breakthrough website, from individuals with Alzheimer's disease and their caregivers, which gave us great inspiration to complete the day's ride. We finally arrived in Santa Cruz at 3:15 PM and gave each other high fives as we celebrated the completion of the first day of the Alzheimer's Breakthrough Ride!
What an amazing day and beginning to the Alzheimer's Breakthrough Ride! I can't wait to follow this Blog as riders move across this great country!
Bruce T. Lamb, Ph.D., is an Associate Staff Scientist in the Department of Neurosciences at the Lerner Research Institute of the Cleveland Clinic, as well as Associate Professor in the Department of Molecular Medicine at the Cleveland Clinic Lerner College of Medicine and in the Departments of Neurosciences and Genetics at Case Western Reserve University. Dr. Lamb also is the Alzheimer’s Breakthrough RideSM Chair and is cycling to raise awareness and make Alzheimer’s disease a national priority. Beginning on July 17, Dr. Lamb and other Alzheimer’s disease researchers participating in the Alzheimer’s Breakthrough Ride will cycle cross-country segments, starting in San Francisco and ending in Washington, D.C. on World Alzheimer’s Day (September 21).
It was a warm, humid, Sunday morning last summer in Cleveland and I decided to go on my usual 30 mile bike ride through the Chagrin River valley. I had just returned from reviewing Alzheimer’s disease research grants for the National Institute on Health and felt increasingly perplexed and concerned regarding the declining funding for Alzheimer’s disease research through the National Institute on Aging (NIA). The percentile of Alzheimer’s disease grants funded through the NIA had dramatically dropped from 2008 to 2009, with further declines anticipated in 2010. Because of this, many Alzheimer’s disease research laboratories were forced to contract in size and some research labs were forced to close all together. Even worse, this meant that critical research that could provide new insights into disease mechanisms and potential therapies for the disease would not be conducted. Given the dramatically increasing incidence of Alzheimer’s disease from the 5.3 million people currently afflicted with the disease to the projected 13.5 million people with Alzheimer’s in 2050, certainly more research is required, not less.
As I started up the first major hill of the ride, my legs burned, my heart pounded and my head ached with indecision about what could be done to bring attention to this critical and unmet need. About half way up the hill, I wasn’t sure I would make it to the top. I finally stood up, slowed down, weaved my way from side to side and inched my way upwards through the steepest grades of the hill. As I reached the top, I realized that a different approach was needed to bring attention and funds to Alzheimer’s disease research, something that involved researchers from across the country united in their commitment to fighting the disease. While researchers frequently complain about funding rates, grant and manuscript reviews and bureaucratic roadblocks to conducting research, rarely do we make the time and effort to raise public awareness of research and advocate for increases in funding. Now is the time, I realized through my heavy, labored breathing, to step up and ride the extra mile and climb the next hill. What if Alzheimer’s researchers from across the country could unite and ride their bikes, from the west coast to the east coast through small towns and big cities, along the oceans and over mountains, reaching out to as many people as possible and finally arriving at the Capitol. Along the way, researchers could convince Americans of the vital role research must play in fighting Alzheimer’s disease. In addition, researchers would get signatures of individuals from across the country in support of increasing funds for Alzheimer’s disease research as proposed in the Alzheimer’s Breatkthrough Act that is currently before congress. It was something that had to be done.
Now, thanks to the involvement of some of the top researchers in the United States and strong organizational support form the Alzheimer’s Association, the Alzheimer’s Breakthrough Ride is a reality. The ride will be starting in July 17th in San Francisco, CA and continuing over 4,000 miles across the country and arriving in Washington, D.C. on September 21st, World Alzheimer’s Day. Today I ask for your support of this important initiative. Get involved, come out to greet and talk with the riders as they come through your community, sign the petition, contact your congressmen and senators and together let’s fight this disease! We have one hardest hill yet to climb and that is Capitol hill.
This week, nearly 4,000 scientists from around the world gathered to report and discuss the latest advances in research on treatments, risk factors, and diagnosis for the health epidemic of the 21st century – Alzheimer's disease – at the Alzheimer's Association's 2010 International Conference on Alzheimer's Disease (AAICAD 2010) in Honolulu.
"With an aging baby boomer generation, the Alzheimer's disease crisis will continue to touch more lives and create an unsustainable fiscal toll on the nation's healthcare system – particularly Medicare and Medicaid," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association.
"This week we saw promising investigations being pursued on a variety of fronts – avenues that could very well lead to significant changes in Alzheimer diagnosis and treatment. However, the chronic underinvestment in Alzheimer research continues to be the greatest obstacle to bringing new, more effective therapies to people," Thies said.
"Every day, researchers go to work with the sole purpose of advancing our understanding and knowledge about Alzheimer's, which is the defining disease of the baby boomer generation. We need a government response that shows equal commitment by providing the level of funding for research that will get us better diagnostic tests, treatments, and a cure," Thies added.
Highlights from the AAICAD 2010 included:
The Alzheimer's Association announced the launch of Alzheimer's Association TrialMatchTM, a confidential, free, and interactive tool that provides comprehensive clinical trial information and an individualized trial matching service for people with Alzheimer's disease and related dementias. The Internet (www.alz.org/trialmatch) and phone-based (800-272-3900) program provides a first-of-its-kind service in Alzheimer's by delivering individualized matches to clinical trials for people with Alzheimer's, their healthcare professionals, caregivers, and healthy volunteers.
The Dementia Demonstration Project (DDP), an interdisciplinary effort led by the Geriatric Research, Education and Clinic Center at the Minneapolis Veterans (VA) Medical Center, found that early detection, diagnosis and care management for people newly diagnosed with cognitive impairment and dementia can reduce outpatient costs by almost 30 percent. Veterans in the study who were diagnosed in the DDP clinics saw their average outpatient healthcare costs decline by an average of $1,991 in the year after diagnosis of cognitive impairment compared with the year before diagnosis. In the DDP clinics, following evaluation, the dementia care team met with the patient and family to review the results, discuss the diagnosis, and outline treatment recommendations. Informational material, assistance in identifying needed services, and direct support and training from team members was provided, as needed.
Evidence from three long-term, large-scale studies (Framingham Study, Cardiovascular Health Study, NHANES III) supports the association of physical activity and certain dietary elements (tea, vitamin D) with possibly maintaining cognitive ability and reducing dementia risk in older adults. Plus, a new study in an animal model of Alzheimer's reported today at AAICAD 2010 suggests that an antioxidant-rich diet with walnuts may benefit brain function. Research has pointed towards a number of factors that may impact our risk of Alzheimer's and cognitive decline, the strongest being reducing cardiovascular risk factors. The Alzheimer's Association and others have repeatedly called for longer-term, larger-scale research studies to clarify the roles that these factors play in the health of the aging brain. These studies from AAICAD 2010 are some of the first reports of this type in Alzheimer's, and that is encouraging, but it is not yet definitive evidence.
Scientists at AAICAD 2010 presented the first draft reports from three workgroups – covering Alzheimer's disease dementia, mild cognitive impairment (MCI) due to Alzheimer's disease, and preclinical Alzheimer's disease – convened by the National Institute on Aging (NIA) and the Alzheimer's Association to update the diagnostic criteria for Alzheimer's disease for the first time in 25 years. The proposals would change the existing criteria by better reflecting the various stages of the disease and the inclusion of Alzheimer's disease biomarkers. While the role of biomarkers differs in each of the three stages, much remains to be understood concerning their reliability and validity in diagnosis. This makes it critical that any new recommendations be thoroughly tested. Further input will be solicited by the NIA and the Association through a website launched immediately after the AAICAD presentations at www.alz.org/research/diagnostic_criteria.
The primary therapeutic target in Alzheimer's disease has been the beta amyloid peptide, which clusters outside cells in the brain to form sticky clumps known as plaques. Recently, more attention has been given to the tau protein, which aggregates inside the brain cells of people with Alzheimer's, forming neurofibrillary tangles. Four new, though very preliminary, research studies reported at AAICAD 2010 described experimental immunotherapies for Alzheimer's – two of which target tau directly and two of which may reduce tau even though their primary target was beta amyloid. Importantly, these studies teach us more not only about tau-targeted therapies but also about the progression of Alzheimer's disease. It may be that amyloid changes in the brain happen early in Alzheimer's, and tau-related changes happen "downstream" where they have a more direct effect on cognitive function. Thus, immunotherapy treatments targeting amyloid may also alter neurodegenerative processes that occur later in the disease. However, this is still to be determined.
In an early finding reported at AAICAD 2010, a gene known as FTO, which appears to be correlated with obesity in humans, may also increase risk of Alzheimer's disease and dementia. When a person has certain variants of both FTO and a recognized Alzheimer's risk gene known as APOE, the risk of Alzheimer's could be doubled. FTO has previously been shown to affect body mass index (BMI) and the risk for diabetes. These vascular risk factors have also been associated with risk of Alzheimer's disease. However, the researchers found that the increased risk was independent of these traits, suggesting that there is a different mechanism by which FTO is associated with an increased risk for Alzheimer's. We need to see these results confirmed by other researchers. In fact, we need to know more, in general, about the genetics and other causes of Alzheimer's so that we have additional targets for therapies and preventions.
Last minute scientific submissions to AAICAD 2010, known as "hot topics," suggested that (1) a newly-discovered risk gene for Alzheimer's may have early impact on memory skills and brain volume, (2) intranasal insulin may be beneficial in Alzheimer's, and (3) beta amyloid deposits in the brains of people with Alzheimer's disease may take different shapes based on a known Alzheimer's risk gene.
Two studies reported at AAICAD 2010 give us more information about the TOMM40 gene – a newly identified risk gene for Alzheimer's. They found that healthy, middle aged people who have the high risk version of TOMM40 (a) did worse on memory tests and (b) had reduced brain volume in two regions affected early in Alzheimer's.
A short-term (4 months) clinical trial of intranasal insulin in Alzheimer's and mild cognitive impairment (MCI) showed statistically significant benefits on certain tests of memory and functioning, but no changes on others. In those who showed benefits on memory tests, there were also positive changes in Alzheimer's biomarkers in spinal fluid. Larger, longer-term studies are planned.
Researchers using a new imaging tool suggest that there are different shapes of beta amyloid deposits in the Alzheimer brain based on which version a person has of a well-established Alzheimer's risk gene, known as APOE. This may be especially important because in some recent drug trials the therapy provided benefits in people who had certain types of APOE but were less effective or not effective in others.
Two new studies from AAICAD 2010 suggest that having Alzheimer's disease may increase the risk of getting other potentially disabling health conditions, including seizures and anemia. Researchers in one study found that that the rate of seizures, per 1,000 people per year, in a study population that included 14,838 people with Alzheimer's aged 50 years or older and 14,838 randomly-selected, age- and sex-matched people without Alzheimer's, was 9.1 among patients with Alzheimer's compared with 1.4 for those without Alzheimer's – an incidence rate that was 6.4 times higher. In a second study of 1,112 older adults (768 healthy controls, 133 MCI, 211 Alzheimer's), people with anemia were found to have an increased risk of Alzheimer's (odds ratio: 2.56). And people with Alzheimer's in the study were found to have an increased risk of being anemic (odds ratio: 2.61). If Alzheimer's also increases risk of other disabling conditions, then its impact may be more devastating than we've envisioned as the global population ages and as more countries become westernized in their habits and lifest
Racially and ethnically diverse older adults are one of the fastest growing population segments in the United States. New research presented AAICAD 2010 revealed that older African-Americans and Latinos with significant cognitive impairment have a lower likelihood of nursing home placement and longer survival than White older adults in the study. These results have significant implications for caregiver burden and community resources. There is a greater than anticipated need for culturally-appropriate dementia care resources and home and community- based services for these populations.
These findings are particularly compelling since African-Americans are about two times more likely and Latinos about one and one-half times more likely to develop Alzheimer's and dementia than Whites, according to the Alzheimer's Association's 2010 Alzheimer's Disease Facts and Figures report.
Another study reported at AAICAD 2010 suggests that the bereavement process and mourning experience for Alzheimer caregivers after the death of their loved one varies greatly among different racial and ethnic groups.
A third research report suggested that cultural and spiritual beliefs of African-Americans, American Indians and Whites greatly influence how long it takes for a family to seek a medical diagnosis of Alzheimer's.
Early detection, diagnosis and care management for people newly diagnosed with cognitive impairment and dementia reduces outpatient costs by almost 30 percent, according to new research reported today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu.
Dementia is loss of memory and other mental abilities severe enough to interfere with daily life. According to the Alzheimer's Association, dementia is a common, costly, and often unrecognized problem in older adults. In order to provide better medical care and outcomes for people with Alzheimer's and other dementias, the conditions must first be detected and diagnosed, and needed care management must be provided.
"Research suggests that when the family of someone who is officially diagnosed with Alzheimer's becomes educated about the disease, and they work together with medical professionals on a care plan, it can reduce the patient's difficult behavioral and psychiatric symptoms," said Maria Carrillo, PhD, Senior Director of Medical and Scientific Relations at the Alzheimer's Association. "It can also lower the family caregiver's anxiety, depression and stress."
Generally, care management in Alzheimer's provides assistance for people with the disease and their families in finding resources, making decisions, and managing stress. For example, a care manager can help families with decisions about in-home health services, or long-term care whether at home or in a nursing facility.
"We see in this study's findings that early diagnosis and case management in dementia may also significantly lower healthcare costs. This could have a reverberating positive impact throughout the entire healthcare system," Carrillo said.
Demonstration Project Shows Early Diagnosis and Care Management Can Lower Costs
The Dementia Demonstration Project (DDP) was an interdisciplinary effort led by the Geriatric Research, Education and Clinic Center at the Minneapolis Veterans (VA) Medical Center. Seven VA Medical Centers took part in the project, which was created to increase detection and diagnosis of dementia in primary care and provide information, support, and care coordination for veterans with newly diagnosed dementia. An Advanced Practice Registered Nurse trained in dementia – the Dementia Care Coordinator – led a dementia care team that became part of a primary care clinic in each of the seven VA Medical Centers participating in the project.
The DDP added a brief, three-item memory test to regularly scheduled primary care visits for veterans age 70 and older without a diagnosis of Alzheimer's or another dementia. Among the 8,278 veterans who received the memory test, 26 percent failed. Thirty-four percent of those who failed the test returned for a comprehensive evaluation; 95 percent of that group were diagnosed with cognitive impairment, including 76 percent with dementia.
In the DDP clinics, following evaluation, the dementia care team met with the patient and family to review the results, discuss the diagnosis, and outline treatment recommendations. Interventions were targeted to the severity of dementia and the specific needs of the patient and their caregivers. Informational material, assistance in identifying needed services, and direct support and training from team members was provided, as needed.
Healthcare costs data for one year before and after diagnosis were available for 347 DDP patients and 1,260 patients from non-DDP clinics in the same VA Medical Centers.
Veterans diagnosed in the DDP clinics saw their average outpatient healthcare costs decline by about 29 percent (-$1,991) in the year after diagnosis of cognitive impairment compared with the year before diagnosis.
Veterans diagnosed in the non-DDP clinics also saw declines in average outpatient healthcare costs, but not as much (-$406).
"In our study, the cost decreases were more dramatic in patients who were identified through cognitive evaluation and who subsequently had case management available by a dementia care team," said J. Riley McCarten, MD, the project's lead physician. He added that the cost of the DDP intervention to the VA was captured in the patient care costs reported.
"The most important goals of the program were making sure that all family members understood the disease and were on the same page, that patients remained physically active and socially engaged, and that caregivers had the support they needed," McCarten said.
-New Alzheimer's Risk Gene May Affect Memory Scores and Brain Atrophy in Middle Age -Clinical Trial of Intranasal Insulin Shows Benefits in Alzheimer's and MCI -Known Alzheimer's Risk Gene May Change Shape of Brain Deposits
Last minute scientific submissions to the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI, known as "hot topics," suggest that (1) a newly-discovered risk gene for Alzheimer's may have early impact on memory skills and brain volume, (2) intranasal insulin may be beneficial in Alzheimer's, and (3) beta amyloid deposits in the brains of people with Alzheimer's disease may take different shapes based on a known Alzheimer's risk gene.
Two studies reported at AAICAD 2010 give us more information about the TOMM40 gene – a newly identified risk gene for Alzheimer's. They found that healthy, middle aged people who have the high risk version of TOMM40 (a) did worse on memory tests and (b) had reduced brain volume in two regions affected early in Alzheimer's.
A short-term trial of intranasal insulin in Alzheimer's and MCI showed statistically significant benefits on certain tests of memory and functioning, but no changes on some others. In those who showed benefits on memory tests, there were also positive changes in Alzheimer's biomarkers in spinal fluid.
Researchers using a new imaging tool suggest that there are different shapes of beta amyloid deposits in the Alzheimer brain based on which version a person has of a well-established Alzheimer's risk gene, known as APOE. This may be especially important because in some recent drug trials the therapy provided benefits in people who had certain types of APOE but were less effective or not effective in others.
"These are some of the fantastic findings from this year's AAICAD, full of potential to move the field forward," said William Thies, PhD, Alzheimer's Association Chief Medical and Scientific Officer. "But there is too little happening in the field, and no plan in place from the federal government to stem the massive wave of Alzheimer's coming with the aging of the Baby Boomers."
"Alzheimer's is clearly the #1 public health challenge of the 21st century and research is the only way to solve this problem," Thies added. "There are more than 5 million Americans with the disease and about 11 million caregivers supporting them. Reliable estimates say that by 2050 those numbers could triple. Government must make an investment in Alzheimer research that proves they understand what's at stake – for individuals, families, the healthcare system, and the nation as a whole."
New Risk Gene for Alzheimer's is Associated with Poorer Memory Function and Grey Matter Loss in Middle Aged Persons Without Dementia
The TOMM40 gene has very recently been shown to influence age of onset in Alzheimer's disease. Two studies reported at AAICAD 2010 give us more information about this newly identified risk gene for Alzheimer's; they found that middle aged people without dementia who have the high risk version of the TOMM40 gene did worse on tests of memory and learning and had reduced brain volume in two regions that are often affected early in the course of Alzheimer's.
"These are exciting, initial results, but the exact role that TOMM40 plays in Alzheimer's remains to be determined," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "The story of TOMM40 is evolving and may give us new insights into Alzheimer's disease."
"We desperately need to know more about the causes of Alzheimer's, and the factors that affect our risk of getting or not getting the disease. This kind of research will provide more targets for therapies and prevention strategies," Thies said.
In one study, Mark Sager, MD, of the University of Wisconsin Medical School, and colleagues studied a total of 726 people in middle-age with a family history of Alzheimer's from the Wisconsin Registry for Alzheimer's Prevention who were genotyped for TOMM40 and APOE, the latter of which is a well-established risk gene for Alzheimer's. Of these, 129 had the low risk version of TOMM40 and 229 had the high risk version. The average age of the study population was 54.
The researchers found that the group with the high risk version of the TOMM40 gene performed significantly worse on the tests of learning and memory (Rey Auditory Verbal Learning Test) than the group with the low risk version. These results remained significant regardless of APOE gene type.
"The deficits shown by the high risk group are similar to the kinds of changes in memory and learning that are seen in very early Alzheimer's," Sager said. "In this study population, TOMM40 genotyping is allowing us to find evidence of very early Alzheimer's disease at least 20 years before people begin to show the outward symptoms. This is a step forward in Alzheimer's prevention research."
In a second study, Sterling Johnson, PhD, also of the University of Wisconsin School of Medicine and Public Health, and colleagues found that among healthy, middle aged adults (mean age 57) who have the APOE e3/e3 gene type, those with the high risk version of the TOMM40 gene had significantly less gray matter volume in two brain regions affected early in Alzheimer's disease than those with the low risk version of the gene.
According to the researchers, the study suggests that there is a connection between TOMM40 and brain cell loss in people who are relatively young and currently not symptomatic.
"This is the first study to associate TOMM40 to brain imaging in people at risk for Alzheimer's disease," Johnson said. "The brain differences between TOMM40 groups were very similar but less severe that what is observed in full-blown Alzheimer's. It may be that the TOMM40 gene will be a useful measure of Alzheimer's risk in middle-age, but additional research with longitudinal follow-up is needed."
Allen Roses, MD, and colleagues at Duke University first discovered that the TOMM40 gene helped explain differences in age of onset among people with sporadic Alzheimer's disease.
Clinical Trial of Intranasal Insulin Shows Some Benefits in Alzheimer's and MCI
Previous research has strongly suggested that Alzheimer's and diabetes/insulin resistance are closely related. For example, Alzheimer's is associated with reduced brain insulin signaling and low levels of insulin in cerebrospinal fluid (CSF).
"These deficiencies may reduce or eliminate insulin's beneficial roles in the brain," said Suzanne Craft, PhD, of VA Puget Sound Health Care System/University of Washington in Seattle. "We believe that restoring normal insulin function in the brain may provide therapeutic benefits to adults with Alzheimer's. Intranasal administration enables insulin to access brain regions that are compromised in Alzheimer's."
Craft and colleagues had previously shown enhanced cognition and daily functioning in adults with MCI and early Alzheimer's using intranasal insulin treatment for 21 days. This new study expanded the time frame to four months, during which 109 participants with MCI or Alzheimer's received either placebo, or 20 or 40 IU daily intranasal insulin treatment.
The researchers found that in the 20 IU dose group (10 IU twice daily) results on a test of delayed story recall significantly improved compared with those who received placebo, as did functional status measured by the Dementia Severity Rating Scale. Improvements in delayed memory recall persisted for two months after the insulin treatment ended. However, memory and learning on the ADAS-Cog and ability to do activities of daily living measured by the ADCS-ADL scores were unchanged.
For 15 of the insulin-treated participants who agreed to have a spinal tap, improved memory and functional status were associated with an improved Alzheimer's biomarker profile as reflected by a lowered CSF tau/Aβ42 ratio.
"These results provide encouraging support for further study of intranasal insulin as a therapy for Alzheimer's," Craft said. "We are currently planning a large, multi-center clinical trial."
New Imaging Compounds for Alzheimer's Protein Deposits in the Brain Show that Different Forms of the APOE Risk Gene Create Different Shapes of Beta Amyloid
A new class of biomarkers has been discovered that can stick to protein structures in the body and emit colors reflecting the different shapes or forms of the proteins. They are called luminescent conjugated oligothiophenes (LCOs) or luminescent conjugated polymers (LCPs). Among other uses, they are currently being employed in test tubes, animal models and autopsied Alzheimer's brains to study the structure of proteins deposits caused by the disease. The new markers bind to the two well-established hallmarks of Alzheimer's – beta amyloid plaques and tau tangles – and glow different colors depending on which forms of the deposits they "stick" to (e.g., plaques often "glow" orange, while tangles "glow" yellowish green).
In this study reported at AAICAD 2010, Sam Gandy, MD, PhD, of Mount Sinai School of Medicine, New York, and colleagues used LCOs/LCPs to investigate the possibility that the shape of brain protein deposits in people with Alzheimer's who have the APOE ε4/ε4 gene type (highest risk) is different from those having APOE ε3/ε3 (neutral risk).
Frozen brain sections from people who died with Alzheimer's were stained using two LCPs/LCOs: pentamer formyl thiophene acetic acid (pFTAA) and polythiophene acetic acid (PTAA). Using PTAA, the researchers observed that Alzheimer patients with APOE ε4/ε4 had core and cerebrovascular amyloid of different shapes, while in people with APOE ε3/ε3 the two amyloid structures had the same shape. Using pFTAA revealed that tau tangle densities in ε4/ε4 Alzheimer patients that were apparently greater than those with ε3/ε3.
"The findings support our hypothesis that APOE genotype changes amyloid structure," Gandy said. "This is important because the different shapes might respond differently to treatments that attempt to clear amyloid deposits from the brain."
In some recent drug trials, the experimental therapy provided benefits in people who had a certain type of the APOE gene (known as ε3) but were less or not effective in another type (ε4).
LCOs/LCPs were pioneered by Peter Nilsson of the Department of Chemistry, Linköping University, Sweden. The study also involved collaborating teams from Charité – Universitätsmedizin Berlin, Germany (led by Frank Heppner), Washington University, St Louis (led by David Holtzman), and other labs at Mount Sinai (led by Patrick Hof and Dara Dickstein).
Scientists at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) today presented the first draft reports from three workgroups convened by the National Institute on Aging (NIA) and the Alzheimer's Association to update the diagnostic criteria for Alzheimer's disease for the first time in 25 years.
The current criteria for the diagnosis of Alzheimer's were established by a National Institute of Neurological Disorders and Stroke (NINDS)/Alzheimer's Disease and Related Disorders Association (ADRDA) workgroup in 1984. These criteria were almost universally adopted and have been useful; they have survived intact without modification for more than 25 years. However, experts note, the field has evolved to a great extent since then.
"Important scientific discoveries have been made in Alzheimer's, and there have been significant changes in our knowledge and conception of the disease," said Creighton H. Phelps, Ph.D., Director of the Alzheimer's Disease Centers Program, Division of Neuroscience, National Institute on Aging at the National Institutes of Health. "The NIA and the Alzheimer's Association, after consultation with the Alzheimer's scientific and medical community, concluded that the diagnostic criteria may need to be revised to incorporate scientific advances. We decided to convene workgroups to examine the literature and make recommendations."
At AAICAD 2010, leaders of the three workgroups – which covered Alzheimer's disease dementia, mild cognitive impairment (MCI) due to Alzheimer's disease, and preclinical Alzheimer's disease – presented preliminary reports at a special session for initial comment by the Alzheimer's community.
"The proposals would change the 1984 criteria by better reflecting the various stages of the disease and the inclusion of Alzheimer's disease biomarkers," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "While the role of biomarkers differs in each of the three stages, much remains to be understood concerning their reliability and validity in diagnosis. This makes it critical that we thoroughly test any new recommendations."
Further input will be solicited by the NIA and the Association through a website launched immediately after the AAICAD presentations at www.alz.org/research/diagnostic_criteria. After that input is incorporated, next steps are publication in a peer-reviewed journal followed by systematic validation through incorporation of the criteria into clinical trials.
"The proposed criteria for Alzheimer's disease dementia must be flexible enough to eventually be used – once they are validated – by both general health care providers without access to neuropsychological testing, advanced imaging, and CSF measures, as well as specialized investigators involved in research or clinical trial studies with access to these measures," said Guy McKhann, MD, of John Hopkins University School of Medicine, who chaired this workgroup.
The Importance of Moving to Earlier Diagnosis
Alzheimer's is thought to begin years, perhaps even decades, before symptoms are noticeable. But there is no single, generally accepted way to identify the disease in its earliest stages – before symptoms are evident.
According to Phelps, earlier detection of people at highest risk for Alzheimer's and those who have the earliest forms of the disease will facilitate finding the right individuals to participate in risk reduction and prevention research studies.
"The NIA and the Alzheimer's Association hope this process of updating and revising the Alzheimer's diagnostic criteria with modern technologies and the latest advances will provide standards that move the field further in the direction of early detection and treatment," Thies said. Significant Advances in Alzheimer Research Since 1984
Among the most important advances in the Alzheimer's field since the publication of the 1984 NINDS/ADRDA diagnostic criteria are:
Alzheimer's-driven changes in the brain, as well as the accompanying cognitive deficits, develop slowly over many years with dementia representing the end stage of years of pathology accumulation. At the same time, we know that some people have the brain changes associated with Alzheimer's and yet don't show symptoms of dementia.
Predictive genes in early onset Alzheimer's indicate that the initial events ultimately leading to both clinical symptoms and pathological brain changes begin with disordered beta amyloid metabolism.
The e4 allele of the APOE gene is well accepted as a major genetic risk factor for late onset Alzheimer's disease, which is defined as onset at 65 or older.
Biomarkers for Alzheimer's have been developed and are being validated. These fall into several categories:
Biomarkers of beta amyloid pathology, including amyloid PET imaging and levels of beta amyloid in cerebrospinal fluid (CSF).
Biomarkers of neuronal injury, including levels of CSF tau and phospho-tau.
Biomarkers of neuronal dysfunction, including decreased uptake of FDG on PET scans.
Biomarkers of neurodegeneration, including brain atrophy on structural MRI scans.
In addition, it has been only in the past decade that a better understanding of the distinctions and overlaps of Alzheimer's with non-Alzheimer's dementias has begun to emerge. Knowledge of the non-Alzheimer's dementias was rudimentary in 1984, and the current diagnostic criteria are vague in defining distinctions between Alzheimer's and the major alternatives. The common co-existence of Alzheimer's and cerebrovascular disease is now appreciated. Much more is known about dementia resulting from Lewy Body disease, and also about Pick's disease and other frontotemporal dementias.
Three Work Group Reports Present New Ideas for Research Criteria and Better Define Early Stages of Alzheimer's Disease
The NIA/Alzheimer's Association working groups were organized around the three stages of Alzheimer's disease that are commonly thought to exist today – pre-clinical Alzheimer's, mild cognitive impairment (MCI) due to Alzheimer's, and Alzheimer's dementia.
Pre-clinical – The group is laying out a research agenda to identify methods of assessment that may help predict risk for developing the disease. Biomarkers and other clinical assessment tools to identify early cognitive decline are being investigated to establish the presence of Alzheimer's brain changes in people with no overt symptoms and to identify those who may eventually develop the disease.
Mild cognitive impairment – The group is refining the MCI criteria, which will help to indicate cognitive change before dementia and better differentiate MCI from Alzheimer's. Research is underway to better understand the cognitive changes taking place, how they may relate to biomarkers, and which of these methods best indicate the likelihood of imminent progression to Alzheimer's dementia.
Alzheimer's dementia – The group is revising the existing criteria for diagnosing Alzheimer's to include possible biomarkers and other assessments that may aid in diagnosis.
Global Impact Could Multiply As The Population Continues to Age
Having Alzheimer's disease may increase the risk of getting other potentially disabling health conditions, including seizures and anemia, according to new research presented today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI.
"Alzheimer's disease is a global health crisis with devastating effects on individuals, families, and national healthcare systems," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "If, in fact, Alzheimer's also increases risk of other disabling conditions, then its impact may be more devastating than we've envisioned as the global population ages and as more countries become westernized in their habits and lifestyles."
According to the 2009 World Alzheimer Report from Alzheimer's Disease International, a London-based nonprofit, international federation of 71 national Alzheimer organizations including the Alzheimer's Association, the number of people with Alzheimer's or another dementia, currently 35 million, is expected to nearly double every 20 years, to 65.7 million in 2030 and 115.4 million in 2050.
Worldwide, the economic cost of dementia has been estimated as $315 billion annually. (Wimo, et al. "An Estimate of the Total Worldwide Societal Costs of Dementia in 2005." Alzheimer's & Dementia: The Journal of the Alzheimer's Association. Vol. 3, Issue 2, April 2007.)
Alzheimer's is Associated with Increased Incidence of Seizures
Some small studies have shown Alzheimer's to be a risk factor for seizures. H. Michael Arrighi, PhD, of Janssen Alzheimer Immunotherapy Research & Development; Nicole Baker, MPH, Pfizer; and colleagues conducted an observational study to estimate the incidence rate of seizures among a large cohort of people with Alzheimer's. The researchers used anonymized electronic medical records from nearly 400 primary medical practices in the United Kingdom. The study population included 14,838 people with Alzheimer's aged 50 years or older and a comparison cohort of 14,838 randomly-selected, age- and sex-matched patients without Alzheimer's. People with Alzheimer's were followed for an average of 2.3 years; non-Alzheimer's patients were followed for an average of 3.4 years.
Over that time period, the researchers found that the rate of seizures, per 1,000 people per year, was 9.1 among patients with Alzheimer's disease compared with 1.4 for those without Alzheimer's – an incidence rate that was 6.4 times higher. In addition, they found that the incidence rate of seizures was highest among the youngest Alzheimer's patients, and that it decreased with age. Incidence among non-Alzheimer's patients increased slightly with age.
"The increased risk of seizures among patients with Alzheimer's disease was seen in all age groups, but there was a substantial increase among the youngest patients. It is especially important for these patients and their caregivers to be aware of this risk," Baker said.
"The connection between Alzheimer's and seizures provides additional avenues for research into the basic biology of both diseases, and possibly interventions and therapies to respond to the overall impact of Alzheimer's disease" Arrighi said.
Alzheimer's is Associated with Lower Hemoglobin Levels and Anemia
Studies suggest that iron accumulates in the tau tangles in the brains of people with Alzheimer's, and that overall levels of iron are elevated in both Alzheimer's and Mild Cognitive Impairment (MCI) brains. However, it is not clear from the scientific literature if this altered brain iron profile is reflected in plasma iron levels.
Noel Faux, PhD, of the Mental Health Research Institute, Parkville, Australia, and colleagues examined hemoglobin, iron and other blood-based measurements in the 1,112 participants (768 healthy controls, 133 MCI, 211 Alzheimer's) of the Australian Imaging Biomarkers and Lifestyle (AIBL) study of Ageing. Participants also completed questionnaires on diet and medication intake (including supplements). Results were then correlated with measures of short-term, long-term and total memory, and global cognition.
The researchers found that people with Alzheimer's in the study had significantly lower levels of hemoglobin, mean cell hemoglobin concentration (MCHC), and packed cell volume compared with healthy controls, after adjustment for age and gender. Consistent with these data, the erythrocyte sedimentation rate (ESR) was significantly higher in Alzheimer's compared to healthy controls.
Participants with anemia in the study were found to have an increased risk of Alzheimer's (odds ratio: 2.56). And people with Alzheimer's in the study were found to have an increased risk of being anemic (odds ratio: 2.61). Self reported iron intake was not different in the two groups.
"In our population, we found that people with Alzheimer's disease were more likely to be anemic, and this was not explained by dietary iron deficiency," Faux said. "This suggests that hemoglobin production is deficient in Alzheimer's patients."
"Alzheimer's had not previously been recognized as a risk factor for anemia, which is a common clinical problem for the elderly and can contribute to problems such as heart failure and renal failure," Faux continued. "The cause of anemia in Alzheimer's is still uncertain, but we speculate that Alzheimer's is a disease that affects both brain and blood. We are currently investigating this intriguing possibility."
Two Target Tau; Two May Reduce Tau Though Their Target Was Amyloid
The primary therapeutic target in Alzheimer's disease has been the beta amyloid peptide, which clusters outside cells in the brain to form sticky clumps known as plaques. Recently, more attention has been given to the tau protein, which aggregates inside the brain cells of people with Alzheimer's, forming neurofibrillary tangles. Precisely how these proteins interact in causing the disease is unclear.
Four new research studies reported today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI describe experimental immunotherapies for Alzheimer's two of which target tau directly and two of which may reduce tau even though their primary target was beta amyloid.
"It is very important that we have a variety of therapeutic targets in the fight against Alzheimer's disease," said William Thies, PhD, Chief Medical and Scientific Officer at the Alzheimer's Association. "The more opportunities that we investigate to intervene and change the relentless and progressive course of Alzheimer's, the better chance that we will find something that works."
"Importantly, these studies teach us more not only about tau-targeted therapies but also about the progression of Alzheimer's disease," Thies added. "It may be that amyloid changes in the brain happen early in the disease and tau-related changes happen ‘downstream' where they have a more direct effect on cognitive function. However, this is still to be determined."
"We need more basic research about what causes Alzheimer's, as well as therapy-related studies, to fill the front end of the drug pipeline and get us the better treatments and prevention strategies that we so desperately need to head off the epidemic of Alzheimer's," Thies said.
Beta Amyloid Immunotherapy with Bapineuzumab in Alzheimer's May Also Reduce Tau
Bapineuzumab (Janssen Alzheimer Immunotherapy and Pfizer) is an antibody to the beta amyloid plaques that are associated with Alzheimer's disease, and is currently in Phase 3 testing as a treatment for mild to moderate Alzheimer's. An abnormal form of the tau protein known as phospho-tau (P-tau) forms into tangles which are the other established lesions in the brain of people with Alzheimer's. The amount of P-tau in cerebrospinal fluid (CSF) is believed to be a marker of active loss of brain cells in people with Alzheimer's; prior studies have shown increases in P-tau in people with mild cognitive impairment who later develop Alzheimer's. P-tau was studied as a therapeutic biomarker in the Phase 2 clinical trials of bapineuzumab.
The pooled exploratory analysis reported at AAICAD 2010 by Kaj Blennow, MD, PhD, of the University of Gothenburg, Sweden, and colleagues included a subgroup of participants from two randomized, multicenter, double-blind, placebo-controlled, multiple-ascending-dose studies conducted in the United States (Study 201) or in the United Kingdom and Finland (Study 202). Study 201 enrolled 35 patients (20 bapineuzumab, 15 placebo) in the CSF substudy, and Study 202 enrolled 11 patients (7 bapineuzumab, 4 placebo) in the CSF substudy. CSF was collected at baseline and 2 weeks after the week 52 infusion.
The researchers found that Study 201 showed a trend (p=0.0564) towards a decrease in CSF P-tau in bapineuzumab-treated compared with placebo-treated cases. In Study 202, no significant treatment effects were seen. When they combined data from both studies, they found a statistically significant decrease (p=0.0270) in P-tau in bapineuzumab-treated compared with placebo-treated patients.
"These observations suggest that immunotherapy treatment targeting amyloid may also alter neurodegenerative processes that occur later in the disease process and that are more directly associated with loss of function," Blennow said. "However, this was a small study and these findings need to be confirmed."
Another Immunization Therapy for Alzheimer's with Beta Amyloid Also Reduces Tau
AN1792 (Elan) showed early promise as a beta amyloid immunotherapy for Alzheimer's. In 2002, a Phase 2 trial reported that about 6 percent of participants developed serious brain inflammation symptoms resembling meningoencephalitis. The trial was stopped as was further clinical development. However, participants in the first AN1792 trial continue to be observed.
Delphine Boche, PhD, of the University of Southampton's School of Medicine, UK, and colleagues studied the levels of beta amyloid and phospho-tau in six regions of cerebral grey matter that are affected by Alzheimer's pathology in the brains of 10 people with Alzheimer's who were immunized with AN1792 and compared the findings with 28 unimmunized Alzheimer cases. They had previously shown a reduction of beta amyloid in people treated with AN1792 and now looked to see if it had any effect on tau.
The researchers found statistically significant reductions in tau and beta amyloid in the immunized patients compared with untreated Alzheimer's. The reduction in tau appeared to be specifically in the dendrites, which are the branched projections of a neuron that conduct the electrochemical stimulation received from other nerve cells to the cell body. In contrast, tau in the bodies of the nerve cells, where the tangles form, seemed unaffected.
"The findings show that treatment aimed at beta amyloid may also modify tau changes in Alzheimer's," Boche said. "The lack of change in tau in the bodies of nerve cells might explain why the people in the original AN1792 trial didn't experience an improvement in cognitive functioning even though we saw amyloid clearance."
"This study demonstrates a link between these two Alzheimer's-related proteins, which has been suspected but not clearly demonstrated in the human brain. The findings give us more basic information about the interaction between beta amyloid and tau in Alzheimer's and may clarify how the disease progresses in the brain," Boche said.
Tau Antibodies Reduce Brain Tangles in Alzheimer-Model Mice
Allal Boutajangout, PhD, of the New York University School of Medicine, and colleagues previously reported that active tau immunization clears tau tangles from the brain and reduces or prevents functional impairments in two different tangle-model mice. In a study reported at AAICAD 2010, they assessed the efficacy of passive immunization for 13 weeks with the PHF1 antibody to tau in a mouse model of Alzheimer's tangles.
The researchers found that weekly injections of PHF1 in the tangle mice reduced the amount of tau aggregates in the brain and decreased functional impairment. The treated mice performed better than controls on the traverse beam task (p<0.03), and had 58 percent less tau pathology in the hippocampus (p=0.02). Plasma levels of PHF1 were inversely related to levels of tau pathology in two brain sections – the brain stem (p<0.01) and motor cortex (p=0.06) – indicating that higher dose of antibodies may have a greater therapeutic effect.
"Targeting hyperphosphorylated tau by immunotherapy is emerging as a promising approach to treat tau-related diseases such as Alzheimer's disease and frontotemporal dementia," Boutajangout said. "Further studies are needed to determine the feasibility of this approach with other tau antibodies and in different tangle models that more closely resemble Alzheimer's."
Alzheimer's Tau Vaccine Shows Promise in a New Rat Model of the Disease
Scientists led by Prof. Michal Novak, MDV, PhD, DSc, of the Institute of Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovakia and Co-Founder and Chief Scientific Officer of the Axon Neuroscience GmbH, Vienna, Austria, have developed a new transgenic rat model of Alzheimer's that, according to Novak, for the first time expresses non-mutated tau and generates Alzheimer's neurofibrillary tangles. Axon is using the rat for early, preclinical development of an Alzheimer's tau vaccine.
In a study reported at AAICAD 2010, Axon transgenic rats were immunized with phospho-tau. The scientists measured changes in functions related to behavior and learning, levels of phosphorylated tau in cerebrospinal fluid, and level of tangle pathology in the rat brains. They found that tau immunization significantly reduced the amount of insoluble tau, prevented development of neurofibrillary tangles, and produced a statistically significant delay of progressive impairment in learning behaviors.
"The Axon Alzheimer Rat may offer new avenues in developing the next generation of therapies and diagnostics for Alzheimer's," Novak said.
- Great need for culturally-appropriate Alzheimer care resources & home-based services -
Racially and ethnically diverse older adults are one of the fastest growing population segments in the United States and new research presented today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu reveals that older African-Americans and Latinos with significant cognitive impairment have a lower likelihood of nursing home placement and longer survival than White older adults in the study.
"These results have significant implications for caregiver burden and community resources," said Maria Carrillo, Ph.D., Alzheimer's Association's Senior Director of Medical and Scientific Relations. "If, as the study suggests, more African-American and Latino families are taking care of their loved ones with significant cognitive impairment in their homes for longer periods of time, there is a greater than anticipated need for culturally-appropriate dementia care resources and home and community- based services for these populations."
"These findings are particularly compelling since we found that African-Americans are about two times more likely and Latinos about one and one-half times more likely to develop Alzheimer's and dementia," Carrillo said. This was reported in March in the Alzheimer's Association's 2010 Alzheimer's Disease Facts and Figures report, a comprehensive compilation of national statistics and information on Alzheimer's disease and related dementias.
Another study reported today at AAICAD 2010 suggests that the bereavement process and mourning experience for Alzheimer caregivers after the death of their loved one varies greatly among different racial and ethnic groups. A third research report suggested that cultural and spiritual beliefs of African-Americans, American Indians and Whites greatly influence how long it takes for a family to seek a medical diagnosis of Alzheimer's.
"Alzheimer's leads so many families through unfamiliar territory. The need for education, information, supportive services is paramount," Carrillo said. "The more we learn about the similarities and differences that exist in how various groups perceive and experience Alzheimer's, the more effective we can be in developing culturally-appropriate information, services, and tools that are respectful of these perceptions and closely held values, and that contain authentic relevance that empowers families." Racial Differences in Nursing Home Placement and Mortality
Few studies have examined how significant cognitive decline impacts minority older adults in the United States. Kala M. Mehta, DSc, MPH, at the University of California, San Francisco, and colleagues examined the relationship between significant cognitive decline and two health consequences – nursing home placement and mortality – in a representative sample of U.S. older adults participating in the Health and Retirement Study. More than 7,500 older people, 10 percent African-American and six percent Latino, were assessed over an 8-year period.
During the study, 23 percent of participants died and 14 percent experienced significant cognitive decline. The researchers found that the proportion of persons with significant decline did not vary by race. However, of those with significant cognitive decline, older African Americans and Latinos had statistically significantly less placement in nursing homes compared to older Whites, and were statistically significantly less likely than similar Whites to die during the follow up period.
"Our results may indicate that African-American and Latino adults have a higher burden from significant cognitive decline than White older adults," Mehta said. "This may impact the adults themselves, their caregivers and their communities. Thus, our findings support the need for culturally-appropriate dementia care, support services and home care resources for African-American and Latino communities in the U.S."
Ethnic Variations in the Bereavement and Mourning Experience
Little is known about the caregiver's bereavement and mourning experience after a family member with Alzheimer's dies. REACH, the Resources for Enhancing Alzheimer's Caregiver Health project led by Richard Schulz, PhD of the University of Pittsburgh's Institute on Aging, provides some of the most comprehensive and systematic information available to date about Alzheimer caregivers.
The Bereavement Component of REACH studied caregivers in three distinct racial/ethnic groups: Hispanics, African-Americans and Whites. James McNally, PhD, of the University of Michigan examined the variations among these groups, including differences in expressions of relief, anger and emotional acceptance.
Study results showed that Whites and Hispanics are three to five times more likely to report a sense of emotional relief at the death of the care recipient, compared to African-Americans. The study also found that Hispanics were only half as likely as African-Americans to report feelings of anger towards the deceased caregivers while White caregivers were considerably more likely to report feelings of anger than both the other groups. Factors such as relationship to the person with Alzheimer's, the emotional and physical health of the caregiver and their sociodemographic characteristics moderated these effects to some degree, but significant differences in the bereavement process remained among the ethnic populations examined.
"For those caring for a family member with Alzheimer's, the process of bereavement often begins long before the family member's physical death," McNally said. "These results bring into sharper focus some distinct social and cultural responses to the bereavement process, and help increase our understanding of the emotional costs of Alzheimer's. This understanding can help to inform and improve culturally competent resources to help caregivers not only throughout all stages of their loved one's illness, but also in finding a healthy resolution to grieving."
Alzheimer's Disease Diagnosis in a Cultural Context
Increasing evidence suggests that early diagnosis of Alzheimer's and timely intervention is beneficial, both for people with the disease and their caregivers. Earlier Alzheimer and dementia diagnosis could allow for earlier use of medications and other interventions that could help to maintain the person's independence longer. Delays in diagnosis also mean that many miss the opportunity to make legal, financial and care plans while they are still capable.
One study of 22 families, including Whites (seven), Blacks (10) and American Indians (five), examined the Alzheimer diagnostic process in a cultural context and found that ethnic minority groups often seek a diagnosis much later than their White counterparts. Led by Peggye Dilworth-Anderson, PhD, of the University of North Carolina at Chapel Hill, the study found that while all groups recognized the value of having a diagnosis, long delays often occurred between family members' recognition of symptoms of dementia and the scheduling of a medical evaluation. The study found that, on average, African-Americans sought a diagnosis six years after dementia symptoms emerged, American Indians sought one after five years, and Whites after two years. Study results also indicated that Whites were more likely to seek support through formal services, while Blacks and American Indians turned more often to their faith and spiritual beliefs for support.
"Many caregivers did not recognize the early signs of dementia because they thought it was a part of their loved one's normal behavior," said Dilworth-Anderson. "Most caregivers mistakenly believed that having dementia is normal and accepted it as a part of growing old. A medical diagnosis of dementia is often only sought after a cultural understanding is developed by the cultural group."
In another quantitative study on dementia care led by Dilworth-Anderson, which involved telephone surveys with 200 Black and White caregivers, about 48 percent of caregivers in the study reported that the care recipient had received a diagnosis of dementia. Among those diagnosed, racial differences in access to care services were observed. Whites reported higher care recipient and caregiver service availability than Blacks, particularly direct care services (such as respite care and caregiving facilities). Blacks reported the use of home health care services for the care recipient more than Whites, and also reported having a greater availability of church resources. Additionally, Blacks reported no services being available at all at a higher percentage than Whites.
- When Combined with a Known Alzheimer's Gene, Your Alzheimer's Risk may be Doubled -
A gene known as FTO, which appears to be correlated with obesity in humans, may also increase risk of Alzheimer's disease and dementia, according to new research presented today at the Alzheimer's Association International Conference on Alzheimer's Disease 2010 (AAICAD 2010) in Honolulu, HI. And when a person has certain variants of both FTO and a recognized Alzheimer's risk gene known as APOE, the risk of Alzheimer's could be doubled.
"While scientists know Alzheimer's involves progressive brain cell failure, they have not yet identified any single reason why cells fail," said Maria Carrillo, PhD, senior director of Medical and Scientific Relations at the Alzheimer's Association. "However, there is evidence about certain factors that may increase the likelihood of developing Alzheimer's."
"Some of these factors we can't control, such as age, family history, and genetics," Carrillo said. "Others we may be able to influence, including heart health, tobacco and alcohol use, and head injury."
FTO has previously been shown to affect body mass index (BMI), leptin levels (a protein hormone that plays a key role in appetite and metabolism), and the risk for diabetes. These vascular risk factors have also been associated with risk of Alzheimer's disease.
In the study reported at AAICAD 2010, Caroline Graff, MD, PhD, and colleagues at the Karolinska Institutet, Sweden, explored the direct role of the FTO gene on Alzheimer's and dementia risk in old age. In addition, a possible interaction of FTO with the APOE gene, a well-established genetic risk factor for Alzheimer's, was assessed. The researchers followed 1,003 people aged 75 years and older without dementia from the Kungsholmen project, Sweden, for nine years to detect new cases of Alzheimer's and dementia. All participants had been genotyped for FTO and APOE on DNA sampled at the beginning of the study.
They found that people in the study population who carried the AA gene-variant in the FTO gene had a 58 percent increased risk for developing Alzheimer's and a 48 percent increased risk for developing dementia compared with those who did not have this genetic variant, after adjustment for age, gender, education, and APOE genotype.
The findings also suggest that the risk-effect of FTO-AA on dementia is further elevated to 100 percent increased risk in the presence of APOE ε4, which is the highest risk variant of the APOE gene. The effect of the FTO-AA genotype on Alzheimer's and dementia risk remained after additional adjustment for diabetes, BMI, cardiovascular disease and physical inactivity.
"One of the intriguing aspects of the results is that the increased risk was independent of the traits previously associated with FTO, such as obesity and diabetes measured at baseline," Graff said. "Our results suggest that the mechanism by which FTO is associated with an increased risk for Alzheimer's and dementia may be different from how it increases the risk for obesity."
"This is a fascinating early finding, which fits with the known connections between heart health and brain health," Carrillo said. "However we do need to see these results confirmed by other researchers. In fact, we desperately need to know more, in general, about the genetics and other causes of Alzheimer's so that we have additional targets for therapies and preventions. One major positive step in that direction would be for the federal government to address its chronic underfunding of Alzheimer's disease research."
The Alzheimer’s Association is the leading voluntary health organization in Alzheimer care, support and research.
Our mission is to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health.
Alzheimer's Association National Office, 225 N. Michigan Ave., Fl. 17, Chicago, IL 60601-7633
Alzheimer's Association is a not-for-profit 501(c)(3) organization
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