Wednesday, July 29, 2015

The coming Alzheimer’s crisis in America

Washington Post
Current quibbling over what Jeb Bush meant when he said it’s time to phase out and replace Medicare — as opposed to “attacking the seniors,” as one woman at a recent event bellowed out — will soon seem quaint against the realities of our future.
Never mind projections that the program will be able to finance only 86 percent of its obligations by 2030. Or that by 2050, the number declines to 80 percent, according to a recently released Social Security and Medicare Boards of Trustees report.
These are relatively comforting numbers compared with new projections from the Alzheimer’s Association. By 2050, the group says, 13.8 million Americans may have Alzheimer’s disease, at a cost of $1.1 trillion per year, mostly to Medicare and Medicaid.
Today, by comparison, 5.3 million have the disease.
“Basically, it will bankrupt Medicare,” said Robert Egge, the Alzheimer’s Association’s chief public policy officer. I met with Egge and chief science officer Maria Carrillo during the association’s recent international conference in Washington.
The 2015 cost of care for Alzheimer’s and all other dementias is estimated at $226 billion, with 68 percent being paid by Medicare and Medicaid, Egge said.
This total includes only direct costs for the care of Alzheimer’s sufferers — there currently is no treatment — and doesn’t take into consideration unpaid care by families. Within the next 10 years, 19 states will see at least a 40 percent increase in the number of people affected.
Lest you feel overwhelmed by numbers — and demoralized by the reduction of human suffering to numerical values — suffice it to say that we are in a state of emergency. Yet, even with this obvious urgency, relatively few resources have been dedicated to research for prevention and treatment compared with other chronic diseases. This, despite the fact that Alzheimer’s is the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention.
Current federal research funding is less than $600 million annually, while top scientists say they’ll need $2 billion a year to meet the association’s 2025 goal of prevention and effective treatment. There’s cause for some hope. Last month, bipartisan House and Senate subcommittees approved increasing funding to the National Institutes of Health for Alzheimer’s research by 50 percent and 60 percent, respectively.
If this funding becomes law — and the association’s goals are met — costs could be reduced by $220 billion over the first five years and $367 billion in 2050 alone, according to an association report. Sixty percent of those savings would accrue to Medicare and Medicaid.
Among other scientific developments reported this week, researchers have isolated a “common ancestor” among all forms of dementia, including Alzheimer’s, Parkinson’s and Lewy body.
“All are caused by misfolding proteins,” Carrillo explained to me. Two different “misfolded” proteins — amyloid beta and tau — are toxic to brain cells.
I am sad to report these proteins cannot be corrected with daily doses of a sturdy zinfandel. There is, however, a new drug that delivers a molecule scientists have created to “chaperone” these proteins so that they fold correctly.
Carrillo doesn’t want to overstate the value of this one-target-one-molecule approach, though it is promising. She suggests that eventually we’ll treat Alzheimer’s with a “cocktail” that will be created based on an individual’s genetic makeup and other factors.
Other hope-inspiring developments include six diagnostic tools that, in combination, can be useful in predicting Alzheimer’s. They include memory and thinking tests, as well as MRI scans that can measure the thickness of the brain’s right entorhinal cortex and the volume of the hippocampus, both of which are important to memory.
It is reassuring that both policymakers and scientists are committed to tackling these diseases. But women especially should be interested in the progress of dementia research. For reasons unknown, women suffer Alzheimer’s at a higher rate — two-thirds of today’s sufferers are women. And women’s function declines twice as fast as men’s. This fall, the association will issue an international call for research on why this is so.
In the meantime, Congress should waste no time in correcting the travesty of too-little funding for a devastating disease that demands our urgent attention. Otherwise, what to do about Medicare will be rendered irrelevant.

Tuesday, July 21, 2015

With millions more expected to develop Alzheimer's, more research funding demanded

I am happy to read more articles that are coming out to share the news of Alzheimer's and its epidemic victims. The key right now is raising more money in hopes of finding a cure and also keeping the exposure along with the momentum going so that individuals understand the cost and this diseases that has zero survivors

Writer for the Los Angeles Times
By: Melissa Healy

Over the next 35 years, about 28 million baby boomers will likely develop Alzheimer's disease, and the annual bill for their care will balloon from $11.9 billion in 2020 to more than $328 billion in 2040, says an analysis released Monday.
Barring the discovery of treatment that could delay or prevent the onset of Alzheimer's disease, the cost of caring for baby boomers with the disorder by 2040 will eat up a quarter of the nation's total Medicare spending, researchers have estimated.
That figure greatly underestimates the true cost of caring for those with Alzheimer's since it does not include out-of-pocket expenses, home care and long-term care insurance payouts, said Maria C. Carillo, chief science officer of the Alzheimer's Assn.
The new projections were presented in Washington, D.C., on Monday at the 2015 Alzheimer's Assn. International Conference. The estimates come from an Alzheimer's Assn. model of the disease's incidence, prevalence and cost of care.
The estimates were used Monday to sound a clarion call for more research funding aimed at finding ways to prevent, delay and treat the disease that progressively robs patients of their memory and their ability to function.
Despite high stakes, candidate-medications on which patients and scientists alike have pinned their hopes have proved ineffective at disrupting or reversing the disease process. Those include wide-ranging efforts to develop drugs that reduce the accumulation amyloid plaques in the brain -- a hallmark of Alzheimer's disease. Researchers in Washington this week are to hear the results of new trials of genetically-engineered therapies that take that approach. But they also will learn whether experimental drugs representing two new approaches to treatment have proved promising in clinical trials.
The escalation of the disease comes as baby boomers -- a generation of 76.4 million Americans born between 1946 and 1964 -- turn 65 at a rate of roughly 10,000 a day.
"The risk of Alzheimer's increases with age, and as baby boomers get older, the number of people developing the disease will rise to levels far beyond anything we've ever seen before," said Keith Fargo, the Alzheimer's Assn.'s director of scientific programs and outreach.
Next year, the oldest baby boomers will begin turning 70 -- an age at which new diagnoses of Alzheimer's jump from less than 1% (among those 65 to 69) to 2.5% (among those 70 to 74). By the year 2050, just over half of baby boomers will be 85 or older, and many with Alzheimer's will have progressed to the disease's most debilitating stages. The cost of care will rise accordingly, the new estimates predict.
Fargo lauded the work of researchers and scientists exploring several promising new approaches to thwarting Alzheimer's. But "Alzheimer's is extremely underfunded compared to the magnitude of the problem," he warned in a speech delivered to researchers and clinicians gathered in the nation's capital.
"If we're going to change the current trajectory of the disease, we need consistent and meaningful investments in research from the federal government to ensure a more robust pipeline," Fargo said. Treatments that have driven down rates of heart disease, cancer and HIV/AIDS infection have benefited from the steady commitment of federal funds, Fargo said.
"Now is the time to do the same for Alzheimer's disease," he added.
The National Institutes of Health are expected to spend $586 million in this fiscal year on Alzheimer's research, and the Obama administration has proposed a $638-million budget for fiscal year 2016. But the planned upward trajectory of spending on Alzheimer's must still make its way through Congress.
The escalating impact of this dementia could be blunted even by therapies that merely delay the onset of Alzheimer's. An Alzheimer's Assn. report released earlier this year estimated that if some therapy were able to delay the average onset of Alzheimer's by five years, the number of people who have the disease in 2050 could drop from 13.5 million to 7.8 million.
The resulting savings could amount to $220 billion over the first five years that such a therapy were in wide use.

Monday, July 20, 2015

New saliva test may catch Alzheimer's disease early

By Liza Lucas, Special to CNN

(CNN) A test detecting Alzheimer's disease early may become easily available thanks to one plentiful bodily substance: saliva, a recently released study shows.
The saliva test was presented at the 2015 Alzheimer's Association International Conference in Washington this week. Though research is still in its infancy, the saliva test represents the exciting future of diagnostic tools in development for the detection of the neurodegenerative disease.
While doctors are currently able to see the difference between a healthy brain and one affected by Alzheimer's, the study emphasizes the importance of detecting Alzheimer's-like changes early.
"As the field has continued to mature over the last decade or so, we now have research and evidence that suggests that the underlying biology of Alzheimer's disease is changing a decade or more before someone experiences the memory or function changes associated with Alzheimer's," said Heather Snyder, director of medical and scientific operations at the Alzheimer's Association.
This test examines saliva samples and looks at changes in saliva as the potential way to detect changes in Alzheimer's, Snyder said.
Researchers from the University of Alberta in Canada analyzed saliva samples of fewer than 100 people, divided into three groups based on cognitive ability: 35 with normal aging cognition, 25 with mild cognitive impairment and 22 with Alzheimer's disease.
    Using protein analysis technology, researchers examined the saliva of each individual, analyzing nearly 6,000 metabolites, which are small molecules that are byproducts of chemical reactions in the brain.
    The team then discovered specific biomarkers (or patterns of metabolites) in the groups with known Alzheimer's or mild cognitive impairment, in comparison with the natural aging group, and tested the biomarkers as predictors of cognitive performance.
    The study was validated through the analysis of a new and independent sample of 27 participants.
    "Salivary metabolomics analyses will advance the cause of early detection of Alzheimer's disease ... and promote our understanding of the mechanisms from normal aging to Alzheimer's," said Shraddha Sapkota, a neuroscience graduate student at the University of Alberta in Canada who presented the study.
    The saliva test is a minimally invasive, as well as cost-effective, way to screen patients early. It allows doctors to identify who is potentially at risk as well as help establish who should be treated and when.
    "Saliva is very easy to collect and transport, which will enhance participation in remote centers and diverse populations," Sapkota said.
    The study was presented at the conference but has not been published or peer-reviewed, which is the gold standard of scientific research. As a result, experts emphasize more research is needed before the saliva test can be used as a detection tool.
    "It is extremely preliminary," said Dr. Dean Sherzai, director of the Alzheimer's Disease Prevention Program at Cedars-Sinai. The samples are so small, the abnormalities could have been incidental, he said.
    "In science, the key is replication," Sherzai added. "[The study] has to be replicated, and it has to be replicated in a larger population."
    While there's no test that conclusively determines whether someone will get Alzheimer's, the saliva test once validated would be a good screening tool, indicating a patient's need for further, more invasive testing. It's especially exciting for Sherzai since it could be used in clinic, or even community, settings.
    "This is important because the earlier you detect this disease," said Sherzai, "the more we can have an effect on the outcome."
    The progressive brain disorder is the sixth leading cause of death in America and affects nearly 5 million Americans. That number is expected to triple by 2050.
    "We have a pressing need to be able to identify people at risk for Alzheimer's disease," said Dr. Richard Isaacson, director of the Alzheimer's Prevention Clinic at New York-Presbyterian/Weill Cornell Medical Center in New York.
    "What we're realizing is that if we can find a drug or some sort of intervention that can slow down or reverse the disease, we'll need to use that drug as early as possible," Isaacson said. "When someone starts having symptoms of memory loss, mild cognitive impairment or dementia due to Alzheimer's, it's so much more difficult to treat."
    Alzheimer's risk reduction and prevention is the new frontier in the disease, according to Isaacson. So the only way to put a dent in the disease is to find some sort of biomarker decades before symptoms start.
    A clinical trial has not been set, but a larger sample study is in the works, according to Sapkota. "We are still at the beginning stages and much work is needed before we can include tests of saliva for the general population," she added.
    Experts say they will be looking for such an easy-to-use, affordable option like the saliva test for the day when that magic pill or drug treatment becomes available.
    "When that blockbuster drug comes," said Isaacson. "A test like this is what we're all looking for."

    Wednesday, July 15, 2015

    2015 San Francisco Chinese Alzheimer's Forum

    Date: Sunday, July 19, 2015
    Time: 1:30 - 4:30 pm
    星期日 1:30 - 4:30 pm  
    The San Francisco Public Library - Koret Auditorium
    100 Larkin Street (at Grove)
    San Francisco, CA  94102  
    A English/ Cantonese Bilingual Health Seminar on Alzheimer's Disease and related dementia, Diagnosis and Care 

    Tuesday, July 14, 2015

    Harri's Tea Company is Giving Back!

    Harris Tea Company is giving back. I happen to think what they are doing is pretty awesome. See the details below!

    Harris Tea Company, a regional branded tea leader located in Moorestown, New Jersey, is as passionate about creating the perfect blend of tea as they are about giving back to the community. Harris Tea’s involvement and support of the Alzheimer’s Association is their best blend yet.
    From June 1, 2015 - May 31, 2016, Harris Tea will donate 5% of proceeds from the sale of their Harris Green Tea, Decaffeinated Green Tea and Decaffeinated Black Tea to the Association with a minimum donation of $25,000. Harris Tea’s generosity will help advance the care, support and research efforts of the Association, moving us closer to our vision of a world without Alzheimer’s.
    Visit to learn more.

    Sunday, July 12, 2015

    A New Alzheimer's Commercial & A Wonderful Documentry

    Check out these links:
    New Alzheimer's Commercial.

    A Woman Story of Early on-set documented.

    A Marriage to Remember | Alzheimer's Disease Documentary | Op-Docs | The New York Times

    Monday, June 22, 2015

    Gene hunter by day, Aerosmith organist by night

    By Jen Christensen, CNN
    Watch "I'll Be Me," the story of 6-time Grammy Award winner Glen Campbell's farewell tour after his 2011 diagnosis with Alzheimer's disease, on CNN Sunday June 28 at 9 p.m. ET.
    (CNN)When Aerosmith looked for an organist to play like a "drunken church lady," they could have taken their pick from hundreds of willing candidates.
    But only one was also a Ph.D-wielding expert on how beta amyloid accumulates in the brain. That's who the band went with for their latest album.
    Legendary Aerosmith lead guitarist Joe Perry met keyboard player and pioneering scientist Rudy Tanzi exactly where you'd expect two world famous people from different worlds to meet -- on a photo shoot for the men's fashion magazine GQ.
    On the shoot, the two started chatting. Tanzi mentioned he played keyboard, so Perry invited him to jam with the band. The two hit it off so well that since then, the Kennedy Professor of Neuroscience at Harvard has been invited to play with Aerosmith on a number of special occasions. His initial direction, he recalled, was to play like a "drunken church lady."
    "It's been such fun," Tanzi said.
    But his true life's work -- or at least the job he is most famous for -- is what he does as director of the Genetics and Aging Research Unit in the MassGeneral Institute of Neurodegenerative Diseases at Massachusetts General Hospital.
      Tanzi is one of the world's leading authorities on Alzheimer's disease. Since the mid-1980s, he has been an unstoppable force trying to understand the genetics of the disease that plagues 5.2 million Americans.
      As in his musical life, Tanzi is known in the lab for his innovative improvisation and for using an unexpected kind of creative thinking. That's why he may be the only scientist in the world who credits early-morning bus rides and watching a cheesy '80s television show as part of his first big break.
      The chromosome 21 guy
      Long before Tanzi was named to the Harvard 100 Most Influential Alumni -- along with such notables as President Barack Obama and Microsoft co-founder and former CEO Bill Gates -- he was just some kid sitting on the back of a bus doing his homework.
      It was the early 1980s, and he was living in Providence, Rhode Island. He kept a grueling daily routine: He'd stay up late playing gigs with his rock band, then rise early to catch a bus to make an hour-plus journey to Boston to work in James Gusella's lab.
      Gusella pioneered the use of DNA sequence polymorphisms as genetic markers at his lab at Massachusetts General Hospital. That essentially means Gusella was one of the first scientist to figure out how to map the genes of a disease.
      "Jim Gusella and I were just kids in our 20s, trying to figure it all out," Tanzi said. "Back then, before genetics became a real industry, you had to jerry-rig everything. To take pictures of DNA, I brought in a Polaroid camera my father gave me for my 13th birthday and I'd put it on a ring stand and I took the red acetate we would use from the light show for my band and it put in the lens. I'd take some of the maps from the dermatology labs to light up the DNA. That was the humble beginning of the human genetics revolution."
      On his bus ride, Tanzi would start his complex calculations. He was trying to build a full map of a chromosome to understand the mechanics of Huntington's disease. "I wanted to get finished fast so I picked the smallest one to map, which is chromosome 21," he said.
      Tanzi says the bus had its regulars with their routines. "They'd be drinking their coffee and get on the bus and say, 'Hey Rudy, how's the map going?' And every day, I'd say, 'Gettin' there. We're gettin' there.' "
      There was no computer program to help back then. So Tanzi did all the tedious work by eye and by hand. "I would sit there with these huge family trees on my papers and I would track genetic markers and I would know who had the disease in the family and who didn't," Tanzi said.
      One night, when he was lying on the red shag carpet back in his Providence apartment, he took out those family trees.
      "I'll never forget I was watching 'Love Boat,' " Tanzi said. "And occasionally I'd look up to seeGopher running around the ship and then look down to write down all the information onto this family tree, then I'd look back up and Gopher was still running around the ship, and then I'd go back to my calculations.
      "After just a little while of doing this I thought to myself, 'My God, this is perfectly lining up. I think we may have found the Huntington's disease gene.' I'm not sure if Gopher ever stopped running around that ship, though."
      It turned out his calculations were right. His work earned Tanzi and his project director some renown.
      "I was just the hands on the project. It was Guesella's brain that made this happen, but it was so cool to actually do the work and to experience this kind of 'aha' moment for the first time," Tanzi said. "Plus, for a while I became known as the chromosome 21 guy, at least for a few years."
      Tanzi was hooked, and his knowledge of chromosome 21 would open more doors to his life's work.
      Stealing who you are
      "Back then there was so much optimism that we could find human genes that cause disease," Tanzi said. Working on chromosome 21 led him to study Down syndrome -- those with the condition have an extra copy of chromosome 21, along with an increased risk for Alzheimer's.
      "So I said, if I have a map for chromosome 21, maybe there's an Alzheimer's gene on this chromosome. So I decided to switch to Alzheimer's," Tanzi said. That was around 1983.
      "And from there I've never turned back."
      At the time, he said, he knew no one with Alzheimer's. "Sometimes in the lab you do these things like you are solving a puzzle and you don't experience the human side," Tanzi said. But only a short time into the work, he got some terrible news.
      His beloved paternal grandmother was becoming increasingly confused. It was soon suspected she had Alzheimer's.
      "It's amazing how as a scientist you become so much more inspired to solve that disease and to work harder and faster by seeing that disease eye to eye, especially in a loved one," Tanzi said. His grandmother quickly went from being friendly and doting to someone who sat stonefaced, unable to recognize her family.
      He says often he will invite families who have relatives struggling with the disease to talk with his students at Harvard.
      "What you see is that this disease is really the worst thing you can imagine," Tanzi said. "Because you spend your whole life -- decades and decades -- accumulating memories and association, and you develop a personality of who you are based on your experience and memories. And this disease comes in and rips all that right out. So it literally steals who you are from you. There is no other disease that does that. There is nothing worse."
      Spurred on by these examples, he worked with urgency. By 1986, all those long hours in the lab paid off.
      "I remember that day," Tanzi said. "We were looking through this one gene we found, and we said, 'Wow, this is matching up pretty well. The protein this gene makes looks exactly like the amyloid that we see in Alzheimer's.' " Amyloid is an abnormal protein that starts to build up in the brain in Alzheimer's cases.
      "When we saw this gene, I remember thinking, 'For the first time since Dr. (Alois) Alzheimerdescribed amyloid in 1906, I think we have finally learned something new about the disease. We now have a gene.' "
      But his celebration was short-lived, he said. "Little did we know that there were three other groups who'd found the gene over the summer of 1986 and we all published at the same time inFebruary of 1987, but it was still a good moment for us. It meant finally now we have a target for drug discovery."
      How to take 'shots on goal'
      Since then Tanzi and his lab have found several other genes related to Alzheimer's, and they are starting to get a clearer picture of how the disease works.
      His lab is a creative place. He tells his students when they walk in the door that they've got to be willing to trust their intuition and to take whatever their pet theory is and try to "bash your hypothesis and see what holds up in the end."
      Even its building is unique -- the lab is tucked in an old brick shipping building. From his window, Tanzi can watch the tourists go by in duck boats, taking pictures as they travel along the Mystic River. His office wall is covered with only a small representation of his many awards, and it is dominated by a beautiful black-and-white photo of his then-baby daughter asleep across his arms while he plays the piano.
      From this office, he strategizes about the next steps in his race to find a cure. He keeps a big red button on his desk that says "no" when pushed. As a joke, he brings it out when his grad students come in to ask for expensive equipment.
      From here, he also makes calls and answers e-mails about his many other projects. There's the New York Times bestseller, "Superbrain," that he co-wrote with new-age doctor Deepak Chopraand the successful PBS show that went with it. There are the small pharmaceutical companies he's co-founded to explore possible Alzheimer's cures and treatments. There is the work he does as chair of the Cure Alzheimer's Fund, which aims to fund new studies concerning the disease. And there is the political consulting he has done with the White House, which has set agoal of curing the disease by 2025.
      Alzheimer's has generated a lot of bad news in the past few years. A number of drug trials have failed recently. The handful of drugs that do exist can slow -- but not stop -- some early symptoms, and even then, only work in less than half the patients. Tanzi, though, believes that with more funding, a cure is possible.
      "In general, drug discovery usually takes two or three waves to get there," Tanzi said. "The first wave already failed. The second wave largely failed, but there is a bit of hope in there. Generally, though, with this third wave that's coming up in the next few years, I think we've learned from our mistakes and I remain optimistic.
      "The good news is, largely due to genetics, we know what we need to do. And we have the information that says 'Here's how we take the shots on goal.' "