Entries in alzheimer's disease (44)


Reading, Writing May Help Stall Mental Decline

iStockphoto/Thinkstock(NEW YORK) -- Dementia, the severe decline in mental abilities, such as memory and reasoning, affects four to five million people in the United States, most of whom are elderly. A study in the journal Neurology finds that keeping the mind active, specifically by reading and writing, can help prevent mental deterioration.

Researchers studied 294 elderly people for six years before their deaths at an average age of 89 and found that those who took part in "mentally stimulating activities" -- like reading and writing -- over the course of their lives had a slower rate of mental decline as compared to those who hadn't.

In fact, those subjects who frequently took part in mental activity late in their lives decreased the decline of their mental faculties by about 32 percent.

Researchers believe that it is important to begin partaking in mental activity during childhood and to maintain it well into your later years.

Copyright 2013 ABC News Radio


NFL Players Risk Death from Alzheimer's Disease, ALS

File photo. Rob Tringali/SportsChrome/Getty Images(NEW YORK) -- Former National Football League players are more likely to die from neurodegenerative diseases like Alzheimer's and ALS, a new study found.

The study of more than 3,400 long-term players between 1959 and 1988 found the risk of death from neurodegenerative disease was triple that seen in the general population, and adds to a burgeoning body of research linking contact sports to chronic brain disease.

"Our results are consistent with those from other studies," said Everett Lehman, an epidemiologist with the National Institute for Occupational Safety and Health in Cincinnati and lead author of the study published today in the journal Neurology. "No one study can make a definitive conclusion about whether concussions cause neurodegenerative disease; the body of literature is what's important."

Of the 334 players who died during the study follow-up, 27 had neurodegenerative diseases that caused or contributed to their deaths, according to the study. The risk of death from Alzheimer's or ALS was nearly four times higher among former NFLers. There was no increased risk of death from Parkinson's disease.

But the players' concussion histories were unknown, raising the possibility that factors other than head trauma might be at play.

"We can't directly link concussions and neurodegenerative disease," said Lehman, explaining how his study relied on death certificates to probe the incidence of neurodegenerative disease. "I think preventing concussions is a logical step to take, but whether that will result in a reduction in chronic neurological disease remains to be determined."

The median age of death from all causes was 54, according to the study.

Previous studies have linked contact sports to chronic traumatic encephalopathy or CTE – a progressive brain disease with features of Alzheimer's, ALS and Parkinson's disease. Lehman said it's possible some of the NFLers in his study had CTE, which can only be diagnosed by a brain autopsy.

"There's no way of knowing," he said. "The symptoms are all very similar."

CTE can also manifest as rage and depression. In February 2011, former Chicago Bears defensive back Dave Duerson fatally shot himself in the chest, leaving a note requesting his brain be sent to the "NFL brain bank" for study. He was later diagnosed with CTE. Former San Diego Charger Junior Seau's brain was also donated to the brain bank after his suicide in May. The results are pending.

Growing awareness of the long term impact of concussions has prompted some former NFLers to sue the league, claiming it downplayed the risks. Other players have signed up to donate their brains to research – a gift they hope will bolster concussion research and protect future athletes.

And the NFL today announced it would donate $30 million to support research on medical conditions affecting athletes, including concussions and late-life neurodegenerative diseases.

"We hope this grant will help accelerate the medical community's pursuit of pioneering research to enhance the health of athletes past, present and future," NFL commissioner Roger Goodell said in a statement. "This research will extend beyond the NFL playing field and benefit athletes at all levels and others, including members of our military."

Copyright 2012 ABC News Radio


Future of Alzheimer's Battle Lies in Prevention, Doctor Says

iStockphoto/Thinkstock(NEW YORK) -- First-degree relatives of adults with Alzheimer's disease have a higher lifetime risk for developing the condition than those without a family history.  However, there is currently little that these relatives can do that is proven to lower their risk of developing the disease later.

It is this problem that Dr. Sam Gandy, professor of Alzheimer's disease research at Mount Sinai School of Medicine, believes will be addressed sooner rather than later.  And he says a new study published in the New England Journal of Medicine Thursday may set the stage for Alzheimer's prevention studies in the near future -- studies that may have more implications for the children of patients than for the patients themselves.

The new study looked at adults who had a genetic form of Alzheimer's but had not yet displayed symptoms.  Interestingly, researchers found that changes in the levels of a protein associated with Alzheimer's, called amyloid, can be detected up to 25 years before symptoms begin.

In an editorial accompanying the new study, Gandy explains why this matters.

"I think this study sets the stage for prevention studies," Gandy tells ABC News. "The only way to know how important amyloid is is to prevent it from forming altogether."

The editorial comes at a time when the potential role of amyloid in Alzheimer's is a topic of growing controversy.  A number of trials for amyloid-lowering drugs failed to show any benefits in patients with mild Alzheimer's.

Gandy argues that these recent drug trials were started too late.  Instead, he argues, new studies should target Alzheimer's prevention, ideally decades before patients show any signs of the disease.  

Hypothetically, the trials could target adults in their 40s and 50s with a family history of the disease.  If a safe amyloid-lowering drug was available, first-degree relatives could potentially get a trial of the drug, and researchers could monitor these individuals to see if they developed Alzheimer's or not.

Most Alzheimer's experts contacted by ABC News agree that the new data is promising.

"In my view, the editorial is precisely on target," says Dr. Paul Aisen, director of the Alzheimer's disease cooperative study at the University of California San Diego.  "This is an important message to share with the scientific community and with families affected by [Alzheimer's] who are discouraged by the disappointing results of large anti-amyloid trials conducted in individuals with dementia."

"Ultimately, to make a real impact, we have to focus on prevention," says Dr. James Galvin, professor of neurology and psychiatry at New York University Langone School of Medicine.  "This means identifying markers of disease to initiate effective treatments before symptoms begin.  Waiting until someone already has memory loss suggests that there is already substantial damage to vital brain systems."

Some experts, however, were more skeptical of the editorial's message.  Specifically, they question whether amyloid is really the true or only culprit behind Alzheimer's -- and whether focusing on it so heavily may close the door too early on exploring other potential factors behind the disease.

"The danger is that if we rely only on the amyloid hypothesis for developing treatment, we might miss other opportunities," says Dr. Zaven Khachaturian, president of the Prevent AD 2020 Campaign.

Copyright 2012 ABC News Radio


Alzheimer's Disease: Should Doctors Prescribe a Skin Cancer Drug?

iStockphoto/Thinkstock(NEW YORK) -- Desperate to stop Alzheimer's in its tracks, some caregivers are clamoring for a cancer drug shown to reverse the disease in mice.  But experts argue prescribing the drug, while legal, is unethical.

"[E]ven if patients and families are willing to take the risks for the potential benefit, the physician's answer should be no," Justin Lowenthal and colleagues from the National Institutes of Health and Massachusetts General Hospital wrote in an editorial published Wednesday in the New England Journal of Medicine.

The editorial was prompted by a February 2012 study published in the journal Science, that found the drug, bexarotene, relieved Alzheimer-like symptoms in three mouse models of Alzheimer's disease.  The drug has yet to be tested in human patients, but because it's approved by the U.S. Food and Drug Administration for a form of skin cancer, doctors can choose to prescribe it off-label.

"Off-label use of medications without proper testing may expose patients and their families to serious side effects without the possibility of benefit," said Dr. James Galvin, an Alzheimer's specialist at New York University.  "In the absence of any human trials, I do believe it unethical to prescribe a medication without evidence of efficacy and safety."

Like other cancer drugs, bexarotene can produce serious side effects, including headaches, hair loss, nausea and depression, and can increase cholesterol levels, according to the National Institutes of Health.  In elderly Alzheimer's patients, many of whom take multiple medications, bexarotene could interact and interfere with other drugs.

Most current medications used in Alzheimer's disease are aimed at symptom relief, addressing problems such as depression, hallucinations, agitation and nutrition.  But bexarotene is thought to attack the disease directly by cleaning up beta-amyloid protein plaques in the brain.  While other treatments targeting beta-amyloid have shown promise in mouse models, they've been largely unsuccessful in humans.

"No mouse data should ever get this kind of ill-advised attention because of a track record of failures," said Dr. Peter Whitehouse, a neurologist at Case Western University in Cleveland.

But for the 5.4 million Americans with Alzheimer's disease and their 10 million caregivers, waiting for human clinical trials is a tall order.  And some doctors say patients and caregivers who understand the risks of an experimental drug should be allowed access.

"If the physician and patient are both suitably well-informed ... an argument could be made that it would be unethical to withhold treatment from a patient who requests it just because the definitive clinical trial had not yet occurred," said Dr. Clifford Saper of Harvard Medical School.

Clinical trials for promising treatments continue, and Dean Hartley from the Alzheimer's Association is optimistic about one day finding a treatment for Alzheimer's disease.

"I think we will find one," he said.  "It's just a matter of when."

Copyright 2012 ABC News Radio


Case Study: IViG Keeps Alzheimer's at Bay for a Decade

iStockphoto/Thinkstock(NEW YORK) -- Jason Marder watched the inevitable decline of his younger brother, who died of Alzheimer's disease at the age of 50.  Then, just after his 60th birthday, he too began to exhibit subtle, early symptoms -- forgetfulness and difficulty focusing on conversations.

The memory loss progressed, and in 2004, Marder got the dreaded diagnosis: Alzheimer's, a disease that affects 5.1 million Americans.

But today, eight years after his diagnosis, Marder isn't any worse off.  He has shown no further memory loss and has remained stable.

Marder credits intravenous immunoglobulin, or IViG, therapy and a clinical trial that is swirling in controversy this week after an announcement of study results by the Alzheimer's Association International Conference 2012 in Vancouver.

Some doctors hailed the therapy as "exciting," something that could potentially stabilize the disease, while others said the research is inconclusive and the study -- with only 16 subjects -- was too small.

Nonetheless, today Marder, now retired from working in apparel, continues his independent lifestyle, playing tennis and biking in his native New York City.

"Things are going really nicely.  I can't complain," said Marder, now 70.  "I don't feel any going backwards."

For the past five years, Marder has been part of a clinical trial with Dr. Norman R. Relkin, director of the Memory Disorders Program at New York-Presbyterian/Weill Cornell Medical Center.

Relkin presented data that found, overall, that 11 study participants who received the immunotherapy Gammagard (IViG) for three full years showed improvements in cognition, memory, daily functioning and mood.

"We are seeing encouraging results," Relkin told ABC News.  And despite negative publicity, "I don't want people to give up hope for symptomatic treatment of the disease".

Intravenous immunoglobulin is a mixture that contains molecules pooled from plasma, a component of human blood.  It is used to treat various autoimmune, infectious and idiopathic diseases, and its supply is therefore limited.

IViG works by using the body's natural defense or immune system and anti-amyloid antibodies.  A protein called beta amyloid accumulates in the brain of those who have Alzheimer's.

"We don't know exactly what it targets, but we do know it contains all antibodies that the body produces," said Relkin.  "It alters the function of the immune system and decreases inflammation in the brain".

He said that his research team found the rate of brain shrinkage had slowed and the study had "exceeded criteria" to go forward with a phase III trial.

Copyright 2012 ABC News Radio


Researchers Discover Uncharted Territory in Pre-Clinical Alzheimer's

iStockphoto/Thinkstock(WASHINGTON) -- This week, at the Alzheimer's Association International Conference in Vancouver, researchers from the Mayo Clinic reported results of their study of potential biomarkers for preclinical Alzheimer's disease.

"Biomarker," a relatively new term in medicine, is a kind of shorthand for the various hints that clue us into the complex ways in which a disease develops. In Alzheimer's disease research, the most studied biomarkers include MRI and PET scan images of the brain.

Their results suggest that among cognitively normal older adults there is a potentially large population who occupy an uncharted territory. Their biomarker results are neither normal, nor clearly abnormal. Dr. David Knopman, the investigator who presented the results, admitted that he and his colleagues "hadn't expected to encounter this result."

One of the biomarkers in question comes in the form of MRI images that show parts of the brain that are atrophied -- areas in which the death of brain cells has "shrunk" the brain. The other set of biomarkers involves two kinds of PET images -- one that measures brain metabolism and the other measures amyloid plaques, which are dense deposits of protein believed to be the "signature" of Alzheimer's disease.

Researchers have embraced these biomarkers because, although they have not discovered what causes this complex disease that develops over a lifetime, they are convinced that discovering its biomarkers is the key to transforming the diagnosis. They hope these advances mean we may one day go from relying on a physician's history and physical exam to determine whether a patient has dementia to a continuum that a physician can diagnose even before a person is ill simply by measuring the presence of so-called "biomarker signatures."

The Mayo Clinic researchers focused on the proposed biomarkers of preclinical Alzheimer's disease, a developing concept that describes individuals who are outwardly normal, but who have the amyloid plaques seen in Alzheimer's disease. Researchers are guessing that, if followed over time, these people will progress to mild cognitive impairment -- notable memory loss with retained ability to engage in day-to-day tasks -- and, ultimately, dementia. Their goal was to use the MRI and PET biomarker results to classify their subjects into the proposed stages of preclinical Alzheimer's disease, follow them for at least a year, and then restage them.

The researchers' assumption was that the stages of preclinical Alzheimer's disease follow a simple stage-by-stage model, meaning, a person moves in a straight line from one stage to the next, beginning when amyloid plaques start to form, progressing to neurodegeneration as seen on MRI or PET scan, and then to subtle cognitive changes.

And that is what they discovered. Their subjects fit into one of the stages and, over time, they moved stage-by-stage as predicted. Over time, nearly half developed cognitive problems that were severe enough a physician diagnosed them with mild cognitive impairment, a condition widely believed to represent an intermediate state between normal aging and dementia.

But the researchers also discovered unexpected territory. As many as one quarter of their subjects did not fit onto their staging map. Instead, they had a mixed biomarker profile. Their brains were not "normal," but they were not clearly "abnormal." These older adults had MRI or metabolic PET scan biomarkers that showed neurodegeneration of an Alzheimer's pattern, but they did not have the pathologic hallmark of Alzheimer's disease. Namely, a PET scan that detects amyloid was entirely normal, a finding that researchers described as "remarkable."

The investigators labeled these people with MRI or PET scans seen in persons with Alzheimer's disease, but without amyloid plaques as having "sNAP," shorthand for "Suspected nonAmyloid Pathway," a name that reveals that we know more about what disease these people do not have than we know about what disease, if any, they do have.

They did not have other common causes of neurodegeneration, including brain vascular disease and Parkinsonism. They were less likely than the subjects who fit into one of the three stages of preclinical Alzheimer's disease to have an APOE4 gene, one of most widely recognized genetic risk factors for developing Alzheimer's disease dementia. Over time, they were no more likely than persons who had no biomarkers to experience cognitive decline.

Persons with this mix of some but not all of the biomarkers of Alzheimer's disease warn us that if we rush to diagnose Alzheimer's disease as early as possible, we could leave as many as one-quarter of patients in a kind of diagnostic limbo. They also challenge the very foundation of the amyloid hypothesis of Alzheimer's disease.

Copyright 2012 ABC News Radio


Is Wobbling Worrisome? Gait Changes May Be an Early Sign of Dementia

iStockphoto/Thinkstock(NEW YORK) -- Slow on your feet? This could be the first sign of memory loss to come.

Three new studies presented Sunday at the Alzheimer’s Association International Conference in Vancouver, Canada, finds that changes in walking patterns of the elderly are closely linked to memory loss and may actually be an early clue to dementia.

One group of researchers studied the strides of a group of elderly patients at Basel Mobility Center in Switzerland.  The study, conducted by lead researcher Dr. Stephanie Bridenbaugh, found that those participants with declines in cognition tended to walk more slowly than their memory-savvy counterparts, particularly when asked to perform a simple task — such as counting backward — while walking.

“Gait analysis can simply, quickly and objectively measure walking,” Bridenbaugh commented in a news release. “When problems emerge, this may provide early detection of fall risk and the earliest stages of cognitive impairment in older adults.”

Other doctors not directly involved with the research agreed that it can be difficult for older patients to perform tasks while walking.

“Someone with mild troubles trying to remember things, they might not be focused as much on walking,” said Dr. William Hu, assistant professor of neurology at Emory University. “I hear this all the time from patients: ‘I was rushing to go to the grocery store, and I left my purse at home.’ Asking a person to do another thing while walking really tests their cognitive reserve.”

Another set of researchers at the Mayo Clinic found similar results. The scientists looked at the changes in the pace and the stride of their patients over the span of 15 months. They found that these changes in walking were directly correlated to their memory loss.

Heather Snyder, senior associate director of the Alzheimer’s Association, reports that these studies “continue to build the evidence that there is a connection between gait and cognition.”

“Gait testing is an inexpensive way for us to observe potential changes,” Snyder said. “It can be done by any physician in their office, as a way to identify people that may need further evaluation.”

Copyright 2012 ABC News Radio


New Drugs Aimed at Ending Alzheimer's Decline

iStockphoto/Thinkstock(NEW YORK) -- The cognitive decline experienced by those with dementia is all too well-known.  And unlike heart disease or cancer, there are no treatments available for the prevention or cure of Alzheimer's, which is a 100 percent progressive and fatal disease.

But that doesn't mean there is no hope.

Alzheimer's researchers and other experts discussed a slew of potential future therapies this week at the Alzheimer's Association International Conference in Vancouver.  The discussions come on the coattails of the U.S. Food and Drug Administration approval of Eli Lily's Amyvid -- a drug designed to help doctors zero in on the toxic culprit believed to cause brain cell death in Alzheimer's disease, a protein called beta-amyloid.

Many of these treatments are in a class of drugs that act in a similar fashion to vaccines, using the body's own immune system to attack beta-amyloid.  Two of these drugs -- Eli Lily's solenezumab and Pfizer's bapineuzamab -- are already in Phase III clinical trials, the last stage of testing before they could potentially be marketed.  Roche's Genentech has also recently been investing in a new drug class that will target another Alzheimer's perpetrator known as tau protein -- a substance released from dead neurons thought to also contribute to the progression of the disease.

"There is a huge revolution going on in medicine using the immune system to target specific abnormalities in the disease pathway of Alzheimer's," said Dr. Michael Rafii, assistant professor of neuroscience at UC San Diego.  Rafii is the associate medical director of the Alzheimer's disease cooperative study, a group that has been testing new Alzheimer's therapies for the last 20 years.  "Immunotherapy has the potential to prevent Alzheimer's disease."

Alzheimer's disease is the most common form of dementia, affecting more than five million Americans, and it is the sixth leading cause of death.  It is caused by an accumulation beta-amyloid, a byproduct of normal brain function.

The human brain is made up of more than 100 billion neurons, and by working together, these neurons are able to create and store a lifetime of hopes, dreams and memories.  Faster and more capable than any computer ever made, the brain has the ability to react to its surroundings in less than two tenths of a second and, scholars have estimated, store more than three million hours of video data.

Normally, our brains are able to get rid of the toxic substance, but in the Alzheimer's brain, the protein accumulates like yellow plaque on un-brushed teeth, eventually leading to the death of brain cells.

Copyright 2012 ABC News Radio


Skin Cells May Offer New Hope for Alzheimer's

iStockphoto/Thinkstock(SAN FRANCISCO) -- A team of scientists has discovered what could be a novel source for researching and potentially treating Alzheimer's disease and other conditions involving the destruction of brain cells.

Researchers at the University of California San Francisco-affiliated Gladstone Institutes converted skin cells from mice and humans into brain stem cells with the use of a protein called Sox2. Using only this protein to transform the skin cells into neuron stem cells is unusual. Normally, the conversion process is much more complex.

Neuron stem cells are cells that can be changed into the nerve cells and the cells that support them in the brain. The neuronal stem cells formed in this study are unique because they were prepared in a way the prevented them from becoming tumors, which is what often happens as stem cells differentiate, explained David Teplow, professor of neurology and director of the Easton Center for Alzheimer's Disease Research at UCLA. Teplow was not involved in the study, but is familiar with this type of research.

These immature brain stem cells then developed into different types of functional brain cells, which were eventually able to be integrated into mouse brains.

The idea that these cells can become fully functioning brain tissue is significant, the authors explained, because by becoming part of the brain, the cells can replace the cells killed off by the disease process.

These cells also offer a potential way to learn about the mechanisms behind neurodegenerative disorders as well as lead to research into new drugs, explained Dr. Yadong Huang, a study co-author and associate investigator at the Gladstone Institute of Neurological Disease.

"The next step is, we are trying to get these skin cells from patients with this disease so we can reprogram and convert the diseased cells into these neuron stem cells and develop those into neurons in culture," he said.

After that, researchers can study how these diseases develop based on what's observed in culture dishes.

"It's really hard to get neurons from human brains for research, and now, we can generate them," Huang said. "Secondly, we can do some drug screening. If we have patient-specific neurons in culture, we can test some or develop some drugs to see how they work on these neurons."

These neuron stem cells, Huang explained, also don't develop into tumors as other types of stem cells are prone to do.

"This is a significant step forward," said Teplow. "Thus far, the challenges with stem cells have been to make the right cells and also be able to make a cell preparation where the risk of having cells that can form tumors is low." Teplow was not involved in Huang's study.

There are still a number of steps this area of research must undergo determining whether these cells can really replace lost brain cells, but experts are encouraged.

"One of the target areas of the brain in Alzheimer's disease is the hippocampus, where there is tremendous loss of neurons, and there is also loss in the outer part of the brain as it progresses," Teplow said. "If we can introduce these cells into these two areas to replenish cells that are lost, we can theoretically reverse the disease."

Copyright 2012 ABC News Radio


Critics Call Government's Alzheimer's Plan Unrealistic

Tom Williams/Roll Call(WASHINGTON) -- The Obama administration and the National Institutes of Health have homed in on Alzheimer's disease, setting an ambitious goal to have an effective treatment for the brain-wasting disease by 2025.

The plan is intended to give a "clear, national focus and attention on Alzheimer's that we've given to other diseases," said Health and Human Services Secretary Kathleen Sebelius in a meeting at the NIH Tuesday.

But Alzheimer's disease experts' reactions to the pledge are less optimistic: Some say giving more attention to the disease can only help, while others call the goal unrealistic.

Most say it is helpful to focus the nation's lens on Alzheimer's, which currently ravages the brains of about 5.4 million Americans and strains 15 million caregivers, numbers that will surely climb as the population ages.

But for some experts, the scope of the government's effort is only a fraction of what is needed to make a difference.

"It's great to have the attention drawn to the disease and have a temporary blip in funding," Dr. Samuel Gandy, a professor of Alzheimer's disease research at Mount Sinai School of Medicine, told ABC News. "But this is at least an order of magnitude off the figure that is likely to have meaningful impact."

The NIH devoted $448 million in fiscal year 2011 for Alzheimer's disease research, compared with the nearly $5.5 billion for cancer research and $3.1 billion for HIV/AIDS. So far, progress against Alzheimer's has been disappointing. There is no cure for the disease, and the treatments that are available only temporarily relieve its symptoms.

Much of the research so far has focused on amyloids in the brain, and whether targeting these protein tangles can prevent or reverse the disease. But answers have been tantalizingly out of reach, despite much research.

"We have had good reason to focus therapies on amyloid, yet they have failed to date. That is discouraging," Dr. Richard Caselli, a professor of neurology at the Mayo Clinic, told ABC News. "So challenge No. 1 is finding good alternative targets."

Dr. Peter Whitehouse, a professor of neurology at Case Western Reserve University in Cleveland, said if the government plan is to succeed, the NIH should broaden its focus on research against Alzheimer's to include more that will help patients cope with the disease or prevent it altogether, such as community design, diet and exercise.

"The field of Alzheimer's research is getting a little distorted. There's a constant need to focus on magic bullets and single molecules," Whitehouse told ABC News. "It really requires a public health focus. The most effective interventions are not going to be drugs."

Other experts defend the government's efforts, saying the plan can only improve current efforts to fight the disease.

"No doubt it's an ambitious goal. What's different now is that we have a goal," said Harry Johns, president and chief executive officer of the Alzheimer's Association.

Sebelius announced new steps in the government's strategy to develop treatments for the disease and provide better support to patients, families and caregivers in the next 13 years.

The first steps include millions in NIH funding devoted to research on Alzheimer's. Two trials will begin immediately -- $8 million for a clinical trial of a potential treatment for early Alzheimer's (an insulin nose spray), and $16 million to study the potential for a treatment to target amyloid, the brain hallmark of Alzheimer's disease, in Colombian people who are healthy but have a genetic mutation that puts them at high risk for developing the disease.

The initiative is part of the National Alzheimer's Plan Act, signed into law by President Obama in January, which marks $50 million for Alzheimer's research in fiscal year 2012 and another $100 million in fiscal year 2013.

According to the Alzheimer's Association, caring for people with dementia cost $200 billion this year alone, and could reach $1 trillion by 2050. The disease is physically and mentally devastating, not just for patients but for families and caregivers who struggle to care for them.

To help embattled caregivers, the government launched, an online resource for patients, families and caregivers looking for information on dementia and where they can get help, and is assigning $26 million to provide resources for patients and caregivers, including support in local communities and a public awareness campaign with TV, radio, online and outdoor ads.

Sebelius said she hoped the government's effort would lead to a strikingly different picture of Alzheimer's disease in the U.S. by 2025.

Copyright 2012 ABC News Radio

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