A call for mainstreaming people with Alzheimer's; 'what's the harm in that?'

As soon as a person is diagnosed with dementia, friends often disappear--even quite early on when the person is just a bit forgetful.

"They think it might all be a bit too awkward," Julian Hughes says of the friends.

"But attitudes must change. Those friends can adjust, let the conversation go with the flow, accept the person with dementia may be living within a few minutes of experience, so you may have to repeat your stories. But what's the harm in that? If they are enjoying it, then it's still a meaningful experience."

Hughes is a British psychiatrist who specializes in aging--his academic interest is the notion of personhood--and recently he spoke throughout Australia, calling for mainstreaming of those with Alzheimer's and other dementias and for governments to recognize this significant health issue. He also made the point that research funding for Alzheimer's lags hugely behind other areas, such as cancer. "As the numbers (of diagnosed) rise, funding will need to increase by a factor of six to eight times to keep pace," Hughes points out.

Dementia is the third-leading cause of death in Australia, behind heart disease and stroke. About 257,000 Australians have dementia today, and that's expected to rise to more than a million by 2050.

In America, deaths from Alzheimer's disease are almost equal to those from diabetes, and both rank below heart disease, cancer, respiratory disorders and accidents. But that's expected to change in the coming years, as Baby Boomers begin hitting age 65. Today, 5.1 million Americans have Alzheimer's disease; that number will climb to 13.5 million by 2050, says a report from the Alzheimer's Association, which says the costs of care will inevitably rise, too, from $172 million today to more than $1 trillion by 2050.

Read the story in The Australian.

Read my previous post about the rising cost of Alzheimer's.

Apple juice found helpful for those with Alzheimer's disease

Behavioral and psychotic symptoms related to dementia seem to improve when people with moderate-to-late stage Alzheimer's disease regularly drink apple juice.

That's what researchers from the University of Massachusetts found in a study published in the June 2010 issue of American Journal of Alzheimer's Disease and Other Dementias.

For their study, the researchers assigned 21 individuals with moderate to severe Alzheimer's disease to drink a 4-oz glass of apple juice twice a day for one month.

Though caregivers reported reduction in anxiety, agitation and delusion, the individuals with dementia showed no changes in the Dementia Rating Scale.

Previous studies have suggested that apple juice may provide health benefits including reduction of central nervous system oxidative damage, suppression of Alzhiemer's symptoms, improved cognitive performance and more organized synaptic signaling. Thomas Shea says other researchers have shown similar effects with blueberries. "We have also shown similar effects with purified vitamins and nutriceuticals." Shea is professor of biological sciences and Director of the Center for Cellular Neurobiology & Neurodegeneration Research at Massachusetts.

Would apple juice be helpful in people with other dementias?

"We saw in mice that apple juice boosted neurotransmitter production, so it might help us all with mood, and the major effect would be seen on those individuals, disease or not, that had behavioral issues," he says. "However, it is certainly worth a try."

Shea says he would like to compare apple juice with apple cider in another study because "cider has the potential benefit of being fresher, and less processed."

Read the article from FoodConsumer.

Read the abstract from the American Journal of Alzheimer's Disease & Other Dementias.

Finding a link between PTSD and dementia raises the question of why

Male military veterans with PTSD were found to have a nearly 2-fold-higher risk of developing dementia, compared to those without post-traumatic stress disorder, an anxiety disorder that is highly prevalent because of combat. Results of a study into this link are published in this month's Archives of General Psychiatry.

The study involved 181,093 veterans 55 years or older without dementia from 1997 through 2000. Between 2000 and 2007, researchers discovered 17 percent of the men developed dementia, according to the abstract by Dr. Kristine Yaffe and colleagues at the University of California, San Francisco, and San Francisco Veterans Affairs Medical Center. They presented their work last year in Vienna at the International Conference on Alzheimer's Disease.

"Mechanisms linking these important disorders need to be identified with the hope of finding ways to reduce the increased risk of dementia associated with PTSD," they write. Some theories: that PTSD contributes to the cause of dementia, that chronic stress plays a role, or that stress damages the hippocampus or cause alterations in neurotransmitter and hormone levels that could precipitate dementia.

Finding a link between PTSD and dementia was not entirely surprising. "We already know that traumatic brain injury and certainly chronic stress increase the risk of cognitive decline and what this paper refers to as 'accelerated aging,' which may in turn lead to early dementia. So it makes sense that PTSD would increase the risk for dementia in the long run," Maria C. Carrillo, a senior director for the Alzheimer's Association, told Medscape.

Read the Medscape article.

Read the abstract from the Archives of General Psychiatry.

Locating genes for clues to Alzheimer's risk, cause, diagnosis

Neuroscientists have zeroed in on some target genes that may be tied to the development of Alzheimer's disease, and they've shown what abnormalities appear on brain scans of people with these genetic variations.

Both bits of scientific progress are incremental steps toward understanding what causes the disease that afflicts more than 5 millon Americans. The study, lead by researchers in Boston and Cambridge, Mass., England and Wales, appears in this month's Archives of Neurology.

"The drought of genetic findings in Alzheimer's disease has lasted a long time," write scientists based in London and Wales in an editorial accompanying the Archives study. "These findings, and the genome-wide studies that presaged them, mark a new period of optimism for those of us who study the etiologies of complex diseases of the nervous system."

The study explains the association researchers made between genetic loci that are related to Alzheimer's disease and neuorimaging measures that are related to disease risk. (These measures include the volume of the hippocampus, amygdala and other brain structures.) They identify B1N1 and CNTN5 as additional specific locations of genetic variants on chromosomes, but say their findings warrant further study.

Just one genetic variant, known as APOE, has been shown to influence Alzheiemer's disease risk and age at onset, lead authors Drs. Alessandro Biffi and Christopher Anderson write in their background information.

Study participants included 168 people with probable Alzheimer's, 357 people with mild cognitive impairment, a precursor to Alzheimer's, and 215 people who were cognitively normal. "Our results indicate that APOE and other previously validated loci for Alzheimer's disease affect clinical diagnosis of Alzheimer's disease and neuroimaging measures associated with the disease," they write.

Will that bring us closer to genetic tests for Alzheimer's?

Somewhat, John Hardy, of the University College London Institute of Neurology, says in an email, "but I think this genetic determinism argument is oversold, frankly.

"About 5 percent of the population are at high risk. About 30 percent of the population are at a moderate risk, and about 65 percent are at lower risk. These numbers are little changed by the new data. And, this is not really so useful for genetic testing."

Read the study in the Archives of Neurology.

The National Institute on Aging's fact sheet on Alzheimer's disease genetics.

Cases of doggy dementia go undiagnosed

Dogs get dementia, too.

It's called canine cognitive dysfunction.

And it's especially interesting, from a research point of view, because canine brains more closely resemble human brains than those of laboratory rats. Also, since so so many dogs are members of human families, they are subject to many of the same environmental factors as humans.

Most senior-age dogs with dementia go undiagnosed, according to a recent study in The Veterinary Journal. Veterinary scientists at the University of Sydney studied 1,000 dogs and found 14 perent had dementia. Only about 2 percent had been diagnosed. (Researchers found no appreciative difference among breeds, by the way.)

''Like dementia in humans, canine dementia often ruins the bond between the sufferer and their carer because the dog no longer seems to recognise the owner or may develop annoying habits,'' Hannah Salvin, a doctoral student at the university who led the study, told the Sydney Morning Herald.

As with humans, the disease is incurable.

Some treatments are emerging, though, and associate professor Paul McGreevy told the newspaper "their responses could provide us with pivotal information about the potential therapeutic effects in humans.''

Salvin and McGreevy are interested in studying more dogs in the greater Sydney area. Their website, maturedogs.com, provides details.

Symptoms

Pacing, circling, wandering.

Failure to recognise familiar people or pets.

Walking into walls or furniture.

Standing over water bowl, not drinking.

Avoiding being petted or touched.

House soiling.

Read the story in the Sydney Morning Herald.

Read the abstract from The Veterinary Journal.

Learn more about Cognitive Dysfunction Syndrome in dogs, from Pfizer.

Research into cognition explains some age-related memory loss

You really can't teach an old dog new tricks. Well, not if you expect the dog to remember the trick.

Through research into cognitive decline, scientists have demonstrated that "there is a biological reason why people cannot learn new things at an older age, but can retain knowledge learned years before," says John Morrison, dean of basic sciences and the graduate school of biological sciences at Mount Sinai School of Medicine.

Certain types of specializations on nerve cells called "spines" are depleted as someone ages, causing cognitive decline in the part of the brain mediating the highest levels of learning, he explains in a study published June 2 in the Journal of Neuroscience.

We lose certain spines as we age, but this study explains which ones and how their loss impacts cognition--which may lead scientists to develop new therapies that target age-related cognitive decline.

The research team studied six young adult and nine older rhesus monkeys as they participated in a delayed response test. The monkeys watched as food was baited and hidden. Then a screen was put in front of them so they could no longer see the location of the hidden reward. At the beginning of the test, the screen was raised immediately, and the monkeys found the reward right away. The memory of the monkeys was tested by increasing the time the reward was blocked from view. The aged monkeys performed significantly worse on the tests than young monkeys, especially as the time intervals increased, researchers reported.

They then studied the microscopic changes in the nerve cells within the prefrontal cortex, an area of the brain that mediates high level learning. Nerve cells in this area contain both thin, dynamic spines which are key to learning new things, as well as large, mushroom-shaped spines that likely mediate long-term memories and expertise. The older monkeys lacked the thin spines but retained the larger spines, "indicating that the loss of the thin spines may be responsible for monkeys' inability to learn and retain information during the test," says a news release from Mount Sinai.

Read the abstract.

Read the article in Science Daily.

A curious study of Agatha Christie and Alzheimer's -- and how our writings may one day be used for diagnosis

The language of people with Alzheimer's disease includes significantly more indefinite words and repetitions than the language of healthy people of similar age and level of education.

So, an English professor at the University of Toronto, Ian Lancashire, analyzed the writing of British mystery writer Agatha Christie.

Previously, the works of British novelist Iris Murdoch were analyzed for signs of the Alzheimer’s disease that was confirmed after her death. Science Blog reported in 2004 that "while the structure and grammar of Murdoch's writing remained roughly consistent throughout her career, her vocabulary had dwindled and her language simplified in her very last novel."

Christie was never diagnosed with Alzheimer's. She continued to write in her final years, though some people believed she suffered from dementia.

Lancashire says her 73rd book, "Elephants Can Remember" is universally dismissed by critics as being full of errors and poorly plotted. The main character is a female novelist who struggles with memory loss while trying to solve a crime that happened in the past.

The professor told National Public Radio that when he read the book, he felt Christie was sensing what was happening to her, and that she kept writing "struck me as heroic."

His study involved feeding the text of 16 of her novels into a computer program that analyzed the vocabulary for the frequency of different words and the number of different words in each novel. "The richness of the vocabulary of Christie’s novels declines with her age at composition. The three novels that she wrote in her 80s, (Nemesis, Elephants, and Postern of Fate,) have a smaller vocabulary than any of the analyzed works written by her between ages 28 to 63," he writes.

Christie was 81 when she wrote the Elephants novel. Her use spiked of what Lancashire called indefinite words--"thing," "anything," "something," "nothing." At the same time, the number of different words Christie used dropped by 20 percent. "That is astounding," Lancashire told NPR. "That is one-fifth of her vocabulary lost."

Most of us don't have large collections of writing done over the course of our lives. But Lancashire points out in his conclusion that "this will begin to change as more individuals begin to keep, if only by inertia, a lifetime archive of e-mail, blogs, professional documents, and the like.

"While the diversity of topics and genres in such an archive brings methodological problems to the analysis ... we can nonetheless foresee the possibility of automated textual analysis as a part of the early diagnosis of Alzheimer’s disease and similar dementias."

Lancashire's paper, "Vocabulary Changes in Agatha Christie’s Mysteries as an Indication of Dementia: A Case Study."

The National Public Radio report.

Factors that may increase risk

Four factors are associated with an increased risk for Alzheimer's disease and cognitive decline. They are not necessarily causes, but science has noticed some meaningful connection between these things and an increased risk for Alzheimer's and cognitive decline. They are:
* diabetes,
* the gene variation ApoE,
* current smoking, and
* depression.

Evidence is not as strong for a connection between estrogens or nonsteroidal anti-inflammatory drugs and an increased risk for Alzheimer's, and there's no evidence of a connection between estrogens or NSAIDS and cognitive decline.

There is also not a consistent association involving cholesterol-lowering medicine, obesity, high blood pressure or blood homocysteine levels for either Alzheimer's or cognitive decline.

Download the 21-page "Preventing Alzheimer's Disease and Cognitive Decline"

state-of-the-science conference statement

Factors that may decrease risk

Three factors are associated with a decreased risk for Alzheimer's disease and cognitive decline. These are not necessarily causes, but meaningful connections. They are:
* cognitive engagement, through literacy and social enrichment,
* physical activity later in life, and
* a diet low in saturated fat and high in vegetable intake.

In addition, light to moderate alcohol intake seems to be associated with reducing the Alzheimer's risk, but not for reducing the risk of cognitive decline.

There is not a consistent association involving the use of gingko biloba, beta-carotene, flavonoids, multivitamins or vitamins B12, C or E.

Read my previous post about what reduces risk (or doesn't)

Download the 21-page "Preventing Alzheimer's Disease and Cognitive Decline"

state-of-the-science conference statement

Can poor vision predict dementia? Untreated, it's associated with cognitive decline

Poor vision that goes untreated is associated with cognitive decline, particularly Alzheimer's disease. Researchers from the University of Michigan, using Medicare data for 625 seniors, found those with vision problems who did not visit an ophthalmologist had a 9.5-fold increased risk of Alzheimer's disease.

”Our results indicate that it is important for elderly individuals with visual problems to seek medical attention so that the causes of the problems can be identified and treated,” says Mary Rogers, PhD. The types of vision treatment that were helpful in lowering the risk of dementia were surgery to correct cataracts and treatments for glaucoma, retinal disorders and other eye-related problems, she says. Rogers is a research assistant professor of internal medicine.

A theory about the association: visual disorders can interfere not only with normal mobility but other activities that may reduce the risk of Alzheimer's disease. These include reading, playing board games, other mentally stimulating activities and social networking.

The university news release.

The abstract from the American Journal of Epidemiology.

Science increasingly links exercise with cognition

I have an appreciation for running. When I'm injured or otherwise unable to run, I feel it--and not just physically. When I run, my mind recharges. It solves problems. It helps me think clearly.

Lenny Bernstein feels similarly. He is the author of an article about how a growing body of evidence links exercise with mental acuity. As a runner, he experiences that cognitive boost, and he writes in The Washington Post : "The tantalizing question for those of us in middle age and beyond (I am 52) is whether this short-term cognitive benefit can be replicated over the long haul. Can exercise help keep our minds sharp? And if so, can it help delay or prevent the truly terrifying mental deterioration of dementia, most commonly seen as Alzheimer's disease?

"Researchers studying both animals and humans increasingly say the answer is yes."

OK, we're not entirely there yet. The link has been observed.

Dr. John Ratey's book, "Spark, the Revolutionary New Science of Exercise and the Brain," ($24.99, Little, Brown and Company) gives lots of examples. It says aerobic exercise has been shown to be as effective as antidepressants; that women who exercise, lower their chances of developing dementia by 50 percent; that a revolutionary fitness program helped put one U.S. school district of 19,000 kids first in the world in science; and that exercise has been shown to spark new brain-cell growth.

"The evidence is incontrovertible: aerobic exercise physically transforms our brains for peak performance," Ratey's promotional materials say. "The major implication is that exercise not only keeps the brain from rotting, but it also reverses the cell deterioration associated with aging," the doctor told the newspaper.

The Washington Post article.

Clinical trials: Should you participate?

Alzheimer's disease and related dementias are still pretty much mysteries. We do not know what causes them. We do not know how to treat or prevent them. The drugs we have treat some symptoms, but not long-term.

Twenty years ago, long before dementia took over his life, my Dad told me about an extraordinary research project that began in 1986. Catholic nuns at Notre Dame had agreed to be studied and tested by researchers from the University of Kentucky. Upon death, all 678 of the sisters agreed that their brains would be analyzed and stored in a laboratory. All of this was in an effort to provide some Alzheimer's answers.

Lots of other studies are underway, that are not so involved. One that I'm aware of looks at whether Gammagard, a drug already used for immune disorders, can preserve thinking abilities in people with mild to moderate Alzheimer's. I found 18 studies having to do with frontotemporal dementia that are currently recruiting people through the U.S. Institutes of Health's clinicaltrials.gov website--which you can search for studies on other types of dementia.

If you or a loved one qualifies for a clinical trial, should you participate? It's something to discuss with your healthcare provider. The National Cancer Institute gives some guidelines, most of which could apply to any trial for any disease. Some things to ask:

How long will the trial last?

Where is the trial being conducted?

What treatments will be used, and how?

What is the main purpose of the trial?

How will patient safety be monitored?

Are there any risks involved?

What are the possible benefits?

What are the alternative treatments, besides the one being tested in the trial?

Who is sponsoring the trial?

Do I have to pay for any part of the trial?

Will I be compensated?

What happens if I am harmed by the trial?

Can I opt to remain on this treatment, even after termination of the trial?

Many people who choose to participate do so for altruistic reasons. Though they may reap some benefit, the real good comes from the incremental contributions they may make toward solving the mysteries of the brain.

Another reason to maintain healthy weight: science connects belly fat and dementia

Being overweight or obese in your 30s puts you at greater risk for developing Alzheimer's later in life, says preliminary research from Boston University's School of Medicine. A study involving 730 subjects showed those with pot bellies in their 30s were more likely to have smaller brains by their 50s--which is associated with a greater risk for dementia.

"Our data suggests a stronger connection between central obesity, particularly the visceral fat component of abdominal obesity, and risk of dementia and Alzheimer’s disease,” Dr. Sudha Seshadri, an associate professor of neurology, told The Money Times. "While preliminary, (our data) provide greater understanding of the mechanisms underlying the link between obesity and dementia."

She told WebMD that the deep fat is the culprit. "We found that subcutaneous was not [significantly] associated with any adverse effect on the brain volume, whereas visceral fat was clearly associated with smaller brain volume." The link was also strong between those with a higher body mass index, and between those with a higher waist circumference.

Article in The Money Times

Story in WebMD

Read the abstract yourself

Good news brewing: Caffeine in coffee seems to reduce amyloid-beta production in Alzheimer's

The caffeine in coffee may have the ability to slow Alzheimer's disease and other dementias, according to Portugese reseachers writing in The Journal of Alzheimer's Disease.

They told ScienceDaily that epidemiological studies showed an inverse relationship between chronic caffeine consumption and the motor deficits and neurodegeneration in Parkinson's disease. Later, similar studies showed a similar relationship between caffeine and Alzheimer's disease. The same has been demonstrated in animal models.

It's early, but researchers--Alexandre de Mendonça of the University of Lisbon and Rodrigo A. Cunha of the University of Coimbra--believe caffeine may prevent brain degeneration, play a role in improving thinking and memory, and protect against Alzheimer's.

Read the studies yourself, (for a fee.)

Some dementias rob taste sensation, too

We know that dementia robs our loved ones of memories and verbalization. Semantic dementia, which affects the temporal lobes, can also take away their ability to discern flavors, according to new research in the journal, Cortex.

Researchers from Washington University and City University London used flavored jelly beans in their study, which The Independent said "shows that the brain plays an integral role in unusual eating preferences and highlights how the brain manages and evaluates flavors and tastes."

"It's quite interesting and unexpected that one would find these sensory signals behaving in the same way words or music might behave," study researcher Jason Warren told MCNBC. "Flavor information is one example of a complex environmental signal that people can lose understanding about, it's part of a more general problem," he said.

Read the MSNBC story.

Read the Science Daily story.

Read the abstract in the journal, Cortex.

5 ways to keep minds young, sharp -- and stave off Alzheimer's

What can we do to keep our brains healthy?

A new book by Paul David Nussbaum, a clinical neuropsychologist at the University of Pittsburgh School of Medicine, provides a recipe for a "brain health lifestyle."

"It does work," he says. "Research suggests if you engage in this type of proactive behavior, you build up brain reserves." A decade ago, science didn't understand that cellular connections in the brain continued to be made at any age, what Nussbaum calls "reserves."

Here's the recipe:

1. Physical activity. Did you know that 25 percent of blood flow from each heartbeat is used by the brain? That's why activity matters so much. Walking, aerobic exercise and dancing are good choices.

2. Nutrition. Our brains are comprised of 60 percent fat. To nourish them, we have to consume the right kinds of fats, unsaturated fats found in foods such as fish. Blueberries and spinach are also good choices.

3. Socialization. Brains that are isolated become lonely. It's important to stay integrated and involved, to have a reason for getting up in the morning.

4. Mental stimulation. We need to keep exposing our brains to things that are new and challenging in order to have a brain that develops brain cells. The more brain cells that we have that connect with each other, the more brain reserve we have. Those reserves can fight off dementia--not prevent it, not cure it, but fight it off.

5. Spirituality. Strong research indicates that chronic stress can lead to memory deficits and perhaps even structural problems in the brain. We combat this by relaxing, meditating and/or praying on a daily basis.

Nussbaum's book is called "Save Your Brain--5 Things You Must Do to Keep Your Mind Young and Sharp" (McGraw-Hill, $16.95.)

The Pittsburgh Post-Gazette story.

KDKA television interview with Nussbaum.

National study underway: Can Gammagard preserve thinking abilities?

A national study is underway to determine if a drug used to treat immune deficiency and autoimmune disorders, Gammagard, can preserve thinking abilities in people with mild to moderate Alzheimer's disease.

Gammagard is made from human plasma and delivered through an intravenous infusion. It contains antibodies against beta-amyloid, which make up the plaques that develop in the brains of people with Alzheimers. A Syracuse neurologist is among the researchers participating in the GAP (Gammaglobulin Alzheimers Partnership) Study paid for by the National Institutes of Health and Baxter Healthcare Corporation, which makes Gammagard.

Find a research site near you.

To join the study, participants must have a mild to moderate Alzheimers diagnosis, be between 50 and 89 years of age and have relatively good health. You cannot enroll if you had cancer within the previous five years or if you take blood thinners.

Participants will continue to take their regular medications and will not know if they are assigned Gammagard through the study. Two thirds will receive the Gammagard infusions once every two weeks. The rest will take a placebo therapy.

After the first three infusions at an infusion center, participants will receive their infusions at their homes. The study continues for 18 months. It also involves office visits, regular blood work and five magnetic resonance imaging studies of the brain. The GAP Study pays for all costs.

The connection between hormone replacement therapy (estrogen) and Alzheimer's

Can estrogen help or hurt a woman's chances of developing Alzheimer's or another dementia?

Scientists are debating just that, and the concept of neuroprotective effects of the hormone remains controversial. Some research suggests it's protective, some that it's harmful depending on the age of the woman and the type of menopause (natural or surgical.)

Dr. Walter Rocca of the Mayo Clinic gives a concise description of "the timing hypothesis" in his abstract for Neurodegenitive Diseases, March 2010.

"Timing" refers to the time at which estrogen supplements are delivered--before, during or after menopause.

Rocca's team reviewed studies already published on the matter and, in some cases, reanalyzed data. They concluded that the neuroprotective effects of estrogen depend on age, type of menopause and the stage of menopause.

They found research suggesting that estrogen could be protective for women taking it in the premenopausal years, commonly before age 50; and also for women in the early postmenopausal phase (commonly from 50 to 60 years of age.) But they found recent trials that showed estrogen treatment initiated in the late postmenopausal phase (ages 65 to 79) led to an increased risk of dementia and cognitive decline.

A 2006 study in Menopause, the Journal of the North American Menopause Society, made the same suggestions--but also said more research is necessary.

The New York Times Magazine recently published a story called "The Estrogen Dilemma" in which the timing hypothesis was mentioned.

Panel: no proof for ways to prevent, slow Alzheimer's

In hopes of staving off Alzheimer's or other dementias, we seek crosswords for mental stimulation, we make it a point to exercise, we down various supplements.

But guess what -- any proof that any of it actually works is lacking.

An independent panel convened by the National Institutes of Health reported that the value of these strategies at delaying the onset or reducing the severity of decline or disease hasn't been demonstrated in rigorous studies. No evidence of even moderate scientific quality supports Alzheimer's risk reduction through dietary supplement intake, use of prescription or non-prescription drugs, diet, exercise, or social engagement, they say.

"Alzheimer's disease is a feared and heart-breaking disease," Dr. Martha L. Daviglus, says in a news release. The panel's chair, she is a professor of preventive medicine and medicine at Northwestern University, Chicago. "We wish we could tell people that taking a pill or doing a puzzle every day would prevent this terrible disease, but current evidence doesn't support this."

Neil Buckholtz from the National Institute on Aging told National Public Radio that "doing crossword puzzles, Sudoku, those kinds of things — they're interesting, but the evidence is not available at this point that they actually have an effect." Evenso, many Alzheimer's researchers say such mental exercise seems like a good idea, since it increases connections in the brain and makes the brain more resilient.

It's certainly not going to hurt.

Now consider: do people stay mentally sharp as they age because they are physically active and socially engaged? Or are they physically active and socially engaged because they are mentally sharp? Daviglus says that's a chicken-or-egg quandary and that such association only tells us the two things are related and not necessarily that one causes the other.

It's the same with some other associations the panel found, between cognitive decline and diabetes, depression, and smoking.

Read the summary from the National Institutes of Health

Read the panel's statement to the NIH.

Exciting discovery suggests protein clumps lead to memory loss in Alzheimer's

Researchers at Mount Sinai School of Medicine say Alzheimer's pathology originates in amyloid-beta oligomers in the brain, rather than the amyloid plaques previously thought by many researchers to cause the disease.

"The buildup of amyloid plaques was described over 100 years ago and has received the bulk of the attention in Alzheimer's pathology, but there has been a lonstanding debate over whether plaques are toxic, protective or inert," lead author Dr. Sam Gandy says in a news release. A professor of neurology and psychiatry, he serves as Associate Director of the Alzheimer's Disease Research Center at Mount Sinai.

The study, paid for by the "Oligomer Research Consortium" of the Cure Alzheimer Fund and a MERIT Award from the Veterans Administration, appears in the journal Annals of Neurology.

Several research groups had previously proposed that rather than plaques, floating clumps of amyloid, called oligomers, are the key components that impede brain cell function in Alzheimer's patients. To study this, the Mount Sinai team developed a mouse that forms only these oligomers, and never any plaques, throughout their lives.

The researchers found that the mice that never develop plaques were just as impaired by the disease as mice with both plaques and oligomers.

"These findings may enable the development of neuroimaging agents and drugs that visualize or detoxify oligomers," Gandy says. That could lead to breakthroughs in managing, slowing, stopping--or even preventing Alzheimer's.

More about oligomerics, from the National Academy of Sciences

The abstract in the Annals of Neurology