A piece of legislation being sponsored by U.S. Senator Charles Schumer would create a "Silver Alert System" to help locate missing adults afflicted with Alzheimer's or other forms of impairment.
The National Silver Alert Act is modeled after the AMBER Alert system, which helps find missing children. The bill would "create a nationwide network for locating missing adults and senior citizens with Alzheimer's, dementia, and other mental impairments," according to a press release.
"When a person with Alzheimer's wanders from his or her home it can be a truly frightening time for that individual and their family and friends," Schumer said. "Statistics show that, with timely notification, the chances of finding a missing person are greatly increased."
More than 60 percent of those suffering from Alzheimer's either wander or get lost while suffering from it, according to the Alzheimer's Association. In addition, 50 percent of those are at risk for a serious illness or even death if they are not located within 24 hours.
"This bill will provide funding for states to set up Silver Alert systems to put more people on the lookout when an adult goes missing to make sure that more families are reunited with their loved ones in New York City and across the country," Schumer said.
The proposed legislation, which has already passed in the House of Representatives, would enable the Department of Justice to create a communications system for Silver Alerts. Along with providing support to Silver Alert programs already in existence, the bill would also "encourage states to develop additional Silver Alert plans."
The bill would provide the Department of Justice with up to $16 million each year for as many as four years to fund grants. The grants would then be used for education, training and needed technology.
Every 70 seconds, someone develops Alzheimer's, and as many as 5.3 million people in the United States are living with the disease, according to the Alzheimer's Association. This progressive, irreversible neurological disorder has no cure, but the earlier someone you love is diagnosed with Alzheimer's disease, the sooner he or she can receive the treatment they need.
That is what organizers hope people will remember on World Alzheimer's Day on Sept. 21. That treatment might include currently prescribed medications or investigational drugs that are being studied in clinical trials.
According to the Alzheimer's Association, memory loss that disrupts daily life is not a typical part of aging. Here are some warning signs the organization suggests could be a symptom of the disease:
1. Challenges in planning or solving problems.
2. Difficulty completing familiar tasks at home, at work or at leisure.
3. Confusion with time or place.
4. Trouble understanding visual images and spatial relationships.
5. New problems with words in speaking or writing.
6. Misplacing things and losing the ability to retrace steps.
7. Decreased or poor judgment.
8. Withdrawal from work or social activities.
9. Changes in mood and personality.
If you or a loved one experiences any of these signs on a regular basis, make an appointment with your physician. If the doctor provides an Alzheimer's disease diagnosis, there are some options to consider.
Clinical trials are the primary way that researchers find out whether a promising treatment is safe and effective for patients. Clinical trials also tell researchers which treatments are more effective than others. Trials take place at private research facilities, teaching hospitals, specialized Alzheimer's disease research centers and doctors' offices.
The biggest benefit of participating in a clinical trial for many families is the regular contact with the study team, according to the Alzheimer's Disease Education and Referral Center. Patients are closely monitored by a medical team that includes a physician.
The team can provide advice on treatment of the emotional and physical aspects of the patient and also help with the caregivers' experience. They can suggest ways to cope and provide insight into what to expect in the future. They also can share information about support groups and other helpful resources.
In most clinical trials, participants are randomly assigned to a study group. One group, the test group, receives the experimental drug. Other groups may receive a different drug or a placebo (an inactive substance that looks like the study drug). Having the different groups is important because only by comparing them can researchers be confident that changes in the test group are the result of the experimental treatment and not some other factor.
Not every patient is right for every trial. But speaking with your doctors, particularly experts in memory disorders, is the first step in understanding the process. They can explain the research procedure in general, as well as which specific program might be the best fit for you.
All trials receive strict oversight from an ethics board, which helps eliminate the worry often associated with clinical trials. According to the Alzheimer's Association, research shows that people involved in studies tend to do somewhat better than people in a similar stage of their disease who are not enrolled, regardless of whether the experimental treatment works. Scientists believe this advantage may be due to the general high quality of care provided during clinical studies.
Today, at least 50,000 volunteers both with and without Alzheimer's are urgently needed to participate in more than 175 actively enrolling Alzheimer's disease clinical trials and studies in the United States. One of these clinical trials that are seeking participants is the ICARA Study, whose goal is to explore if an investigational drug, called bapineuzumab, can help slow the progression of Alzheimer's disease. For more information about this trial, visit www.icarastudy.com or call (888) 770-6366.
ScienceDaily (Oct. 29, 2009) - Researchers in the USA have discovered a potential new function for anti-epileptic drugs in treating neurodegenerative disorders such as Alzheimer's and Parkinson's disease. The study, published in BioMed Central's open access journal Molecular Neurodegeneration, found that neurons in the brain were protected after treatment with T-type calcium-channel blockers, which are commonly used to treat epilepsy. Calcium signaling pathways play a vital role in the survival of neurons in the brain. As age increases, calcium homeostasis can be disrupted in the brain, which may lead to cognitive and functional decline. It therefore raises the possibility that chemicals able to modulate calcium homeostasis could protect neurons.
Jianxin Bao and colleagues, from Washington University, Missouri, USA, were one of the first teams to explore the possible protective effects of blockers for T-type calcium channels. The mechanisms for neuroprotection by these antiepileptic drugs were previously unknown. Bao's team established cell culture models to directly test whether these drugs could preserve neurons in long- and short-term cultures in vitro.
They found that neurons showed an increase in viability after treatment with either L-type or T-type calcium channel inhibitors. Furthermore, neurons in the long-term and short-term cultures were protected, respectively, by L-type and T-type calcium channel blockers, suggesting that more than one calcium-signaling mechanism exists to regulate long- and short-term neuron survival.
There are presently no effective medications for age-related neurodegeneration. Bao said: "Our data provides implications for the use of this family of anti-epileptic drugs in developing new treatments for neuronal injury, and for the need of further studies of the use of such drugs in age-related neurodegenerative disorders."
Norelle C Wildburger, Avary Lin-Ye, Michelle A Baird, Debin Lei and Jianxin Bao. Neuroprotective effects of blockers for T-type calcium channels. Molecular Neurodegeneration, 2009; (in press)
ScienceDaily (Oct. 28, 2009) - Research has shown that diabetes increases the risk of Alzheimer's disease and the risk of memory loss in people who don't have Alzheimer's disease. But it hasn't been clear whether people with Alzheimer's disease and diabetes have more rapid memory loss than those who have Alzheimer's disease but no diabetes.
New research published in the October 27, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology, suggests that those with both diseases actually have a slower rate of memory loss than people who had only Alzheimer's disease.
"This result was surprising," said study author Caroline Sanz, MD, of INSERM, the French National Institute for Health and Medical Research in Toulouse. "Our initial hypothesis was that diabetes would increase the rate of cognitive decline in people with Alzheimer's disease."
For the study, researchers followed 608 people with mild to moderate Alzheimer's disease for four years and tested their memory and thinking skills twice a year. A total of 63 people, or 10.4 percent, had diabetes.
At the beginning of the study, both those with and without diabetes had average scores of 20 points on the cognitive test. Over each six-month testing period, the overall group declined by an average of 1.24 points on the test. However, those without diabetes declined by 0.38 points more per six-month period than those with diabetes.
Researchers say it is not clear yet why the rate of memory loss was slower for people with diabetes. "One possible explanation is that diabetes in the elderly differs from that in younger people and in addition, elderly people with diabetes may be more likely to receive cardiovascular medications such as drugs for high blood pressure than people who don't have diabetes," Sanz said. "These drugs have been reported to decrease the risk of developing Alzheimer's disease and also the rate of cognitive decline in people with Alzheimer's disease. Other possible explanations for these findings may relate to differences in brain lesions in those people with diabetes compared to those without diabetes."
The study was supported by the French Ministry of Health and the Toulouse University Hospital.
Adapted from materials provided by American Academy of Neurology.
ScienceDaily (Oct. 27, 2009) - Sometimes when a patient tells his ophthalmologist that he "can't see," what he really means is "I can see, but I can no longer read or write." In a minority of Alzheimer's patients the disease shows up first as problems with vision rather than memory or other cognitive functions. But diagnosis can be difficult because standard eye exams are often inconclusive for these patients.
Neuro-ophthalmologists Pierre-Francois Kaeser, MD, and Francois-Xavier Borruat, MD, Jules Gonin Eye Hospital, Switzerland, examined and followed 10 patients with unexplained vision loss who were ultimately diagnosed with the visual variant of Alzheimer's disease (VVAD). Their study -- presented at the 2009 Joint Meeting of the American Academy of Ophthalmology and the Pan-American Association of Ophthalmology (PAAO) -- describes clinical clues that may improve ophthalmologists' ability to detect VVAD and refer patients for further tests. When patients receive neurological assessment, treatment and family counseling early in the disease, outcomes may be better for all concerned.
VVAD patients differ from typical Alzheimer's patients in a number of ways. At the time they report visual problems, many are younger than those for whom memory loss is the tell-tale sign. In Dr. Kaeser's study the median patient age was 65, and only 3 of 10 reported memory loss. In comprehensive neuro-ophthalmic exams even though most patients' visual acuity was adequate, all but one had difficulty with reading, 8 of 10 with writing, and 6 of 10 with basic calculations. The visual field was altered in 8 of 10 patients.
All had trouble identifying colored numbers despite being able to name colors correctly, and, importantly, 8 of 10 patients had difficulty recognizing and interpreting components of a complex image (simultagnosia). This is an early indicator of the brain damage that prevents later-stage Alzheimer's patients from recognizing people they know and navigating familiar surroundings. MRI and PET scans revealed neurological changes consistent with VVAD in all study patients. Though VVAD patients' first symptoms are visual, Alzheimer's memory and personality impairments eventually occur in most.
"Ophthalmologists should be aware of the possibility of VVAD in patients with unexplained vision problems, particularly difficulty with reading," said Dr. Kaeser. "Suspect VVAD when patient tests well for visual acuity but has vision complaints that are unusual or severe for late middle age. Refer him for neurological evaluation."
Adapted from materials provided by American Academy of Ophthalmology, via EurekAlert!, a service of AAAS.
Can you catch Alzheimer's disease?
Controversial theory links the memory-erasing condition to herpes virus
By Tom McGrath
updated 10:20 a.m. CT, Sun., Oct . 25, 2009
Rich P. is only in his 20s, but these days he finds himself obsessing over something most guys his age never think twice about: Am I doomed to lose my mind?
In some ways, Rich's anxiety is understandable. "My girlfriend is a social worker who works with the aged, specifically people with Alzheimer's," he says. "So I've seen close up what the disease does to you." Indeed, Alzheimer's disease is characterized by memory loss and confusion, and typically ends with complete disconnection from the world. People in its advanced stages can't care for themselves, recognize loved ones, or remember the lives they lived. (Worried about losing your memory and health as you age? Discover the age erasers for men that can strip away 10 years and leave you looking and feeling younger, longer!)
There's also another, even more personal connection for Rich: His girlfriend's father recently passed away from Alzheimer's. He was one of more than 70,000 Americans who die from the disease every year.
Still, what should worry Rich most isn't what he's witnessed in other people, but what he sees in the mirror. Because there, literally right under his nose, is evidence that the monster that could be responsible for Alzheimer's is already skulking about inside his body, preparing itself-at some point, decades down the road-to attack and destroy his brain.
So here's the question: Is it in you, too?
For years, physicians and Alzheimer's experts have said that the earliest symptoms of the disease typically don't appear until you're in your 60s, 70s, or beyond. But now there's reason to believe that the first warning signs may actually crop up much earlier than that, and in a seemingly much more benign way: as cold sores, those embarrassing blisters that can erupt on the lips of people who are sick or run-down.
The sores are triggered by the herpes virus - most often, herpes simplex virus type 1 (not to be confused with HSV-2, which predominately causes genital herpes). In recent years, a growing body of research, much of it championed by a British scientist, has begun to suggest a startling fact: The same virus known for sabotaging people's social lives could be responsible for the majority of Alzheimer's cases.
"There's clearly a very strong connection," says the researcher, Ruth Itzhaki, Ph.D., speaking one afternoon in her office at the University of Manchester, in northwestern England. A neurobiologist, Itzhaki has spent the better part of two decades studying the link between herpes and Alzheimer's. "I estimate that about 60 percent of Alzheimer's cases could be caused by the virus."
As viruses go, herpes is a particularly devilish bugger. The ancient Greeks were among the first to record the sores it causes (the virus's name is derived from a Greek word meaning "to creep"), and today the microbe is ubiquitous. As many as 85 percent of us have been infected by it, though experts say as few as 15 percent show symptoms. Worse, once you have it, you have it forever: After the initial infection, the virus lies dormant in your peripheral nervous system, occasionally flaring up during periods of stress, illness, or fatigue. You can follow these three steps to prevent a herpes outbreak, but it never completely disappears.
And it's that fact - herpes as the viral equivalent of The Thing That Wouldn't Leave - that lies at the heart of the herpes-Alzheimer's relationship. Research suggests that as we age, HSV-1 actually spreads to our brains, where in certain people, Itzhaki theorizes, it can cause the buildup of deposits - known as amyloid plaques and neurofibrillary tangles - that attack and destroy the cells responsible for memory, language, and physical functions. In short, those people develop Alzheimer's.
It's a provocative theory, one that would sound preposterous if it weren't for the steadily accumulating evidence. Last January, for instance, Itzhaki and her colleague, Matthew Wozniak, Ph.D., published a study in the Journal of Pathology in which they searched for the presence of the herpes virus in people's brains. They found that it resided in 90 percent of the amyloid plaques.
"The link between herpes and Alzheimer's has been there for a while, but more people are starting to pay attention," says Howard Federoff, M.D., Ph.D., an expert on neurodegenerative diseases and the executive dean of the school of medicine at Georgetown University. "It's no longer just a curiosity."
The cold sore connection
Unfortunately, while the theory may be on more researchers' radar, it's perhaps becoming a blip in the one area that matters most: the fight for funding. Sure, on the surface, the possible discovery of a cause for Alzheimer's looks like Nobel-caliber news because it suggests a way forward in treating a disease that scientists have struggled - largely unsuccessfully - to understand. What's more, if a new treatment does emerge, it could be just in the nick of time: Thanks to a combination of changing demographics and longer life spans, experts are predicting nothing less than an Alzheimer's epidemic in the decades ahead.
And yet all the promise held in the herpes connection may vanish as quickly and completely as the memories of an Alzheimer's patient. That's because despite Itzhaki's nearly 20-year struggle to get her work noticed, an entrenched Alzheimer's research establishment remains skeptical. Worse, she now finds herself on the brink of having to shut down what may be the most promising avenue of investigation in ages.
"Our remaining funds are sufficient for only several more months," she says, "so unless we obtain a donation or grant, the work will then stop completely, because nobody else in the world is directly doing such research."
For young men like Rich P., who wonders what's in store for him in the decades ahead, this would appear to be an enormous scientific misstep - particularly since Rich believes he's seen firsthand the link between herpes and Alzheimer's.
His girlfriend's father, the one who passed away from Alzheimer's? He battled cold sores all his life.
Itzhaki says there are two reasons why herpes became a Virus of Interest in the hunt for an Alzheimer's cause. First was the observation, almost three decades ago, that a rare infection called herpes encephalitis affects the same regions of the brain that Alzheimer's does. Like people with Alzheimer's, encephalitis patients can be plagued by memory problems. (Read about the latest research on the secrets of your brain and how to preserve your memories here.) The other factor, she says, is the prevalence of the herpes virus itself.
"Most people get it as children," Itzhaki says. "It's in your saliva, and it can easily be passed along with a kiss from a family member." She says it's not really that puzzling that most people who carry the virus never show symptoms - as she puts it, not everyone who's infected with a microbe is necessarily affected by it. "It depends on the person harboring the virus," she says. "It's probably based on genetic factors."
How might a germ you could have contracted from, say, a grandparent potentially destroy your brain when you become a grandparent?
In the early 1990s, researchers, including Itzhaki, found evidence suggesting that as we age, the herpes virus begins moving from its hideout near the bottom of the skull directly into the brain (possibly because our immune systems lose some bite). Indeed, one Journal of Pathology study found the virus in a high proportion of postmortem brain samples taken from people who'd died in their later decades, while it was absent in those from people who'd died in youth or middle age.
What effect does the virus have when it reaches your brain? The short answer: That depends. In certain people it seems to do much less damage than in others; just as some of us never develop cold sores, some of us can have the herpes virus inside our brains without any horribly ill effects. But Itzhaki believes that in other people - specifically those who carry APOE e4, a gene form, or allele, strongly linked to Alzheimer's - the virus is not only reactivated by triggers like stress or a weakened immune system, but also actually begins to create the proteins that form the plaques and tangles presumed to be responsible for Alzheimer's.
If you're looking for evidence, Itzhaki can show you a stack of it. In two studies, for example, she and several colleagues took brain samples from 109 deceased people - 61 of whom had had Alzheimer's, 48 of whom hadn't - to search for any correlation between herpes, APOE e4, and Alzheimer's. Their results: People who had both the APOE e4 gene and the herpes virus in their brains were 15 times more likely to have Alzheimer's than people who had neither. (The researchers also found, intriguingly, that people who suffered from recurrent cold sores were almost six times as likely to have the APOE e4 gene as those who didn't get cold sores.)
A decade later, Dr. Federoff, then working at the University of Rochester, administered the herpes virus to four different groups of mice, each of which had a different variation or absence of the APOE gene. He found that in mice with the specific APOE e4 variation, the virus was slower to become dormant than it was in mice with APOE e2, APOE e3, or no APOE gene, suggesting that the virus could be replicating faster in the e4 mice. "The results definitely suggest there's something different about having APOE e4," says Dr. Federoff.
Still other research shows the direct impact of HSV-1 itself. In 2007, a study by Itzhaki and Wozniak found that infecting lab samples of brain cells with the virus caused a buildup of the protein (beta amyloid) that's the primary component of the plaque clogging the brains of Alzheimer's patients. The same study also found a similar result in the brains of mice that had been infected with HSV-1.
Then there was January's study in the Journal of Pathology. In it, Itzhaki and Wozniak looked at brain samples from 11 deceased people; six had had Alzheimer's and five hadn't. While both groups had plaques (not surprisingly, the Alzheimer's group had far more) and evidence of the herpes virus in their brains, there was a crucial difference in the concentration of the virus: In the Alzheimer's patients, 72 percent of the virus's DNA was found in the plaques, compared with only 24 percent that was found in the plaques of the non-Alzheimer's brains. Not surprisingly, all but one of the Alzheimer's sufferers also carried the APOE e4 gene, compared with none of the samples from the non-Alzheimer's people.
Wozniak is confident that these last two studies point to the same conclusion: "The results strongly suggest that HSV-1 is a major cause of amyloid plaques - and probably of Alzheimer's disease."
For Wozniak and Itzhaki, the next step is to test whether antiviral drugs like Zovirax and Valtrex, both of which are used to shorten the duration of cold sores, might alleviate or slow the progression of Alzheimer's. The pair is seeking funding for two experiments with antiviral drugs - one testing them on mice, the other testing them on Alzheimer's patients.
"If the treatment is successful, it would stop progression of the disease, rather than just stopping the symptoms," Itzhaki says.
But that funding isn't likely to materialize if the rest of the research community continues to dismiss Itzhaki's theory - or ignore it altogether. When I e-mailed John Trojanowski, M.D., Ph.D., a respected Alzheimer's researcher at the University of Pennsylvania, to find out his take on the connection between Alzheimer's and herpes, he shot back a one-sentence reply: "Do not know of any connection."
When I pressed and asked him to take a look at two of Itzhaki's recent studies, he was equally dismissive. "This is an old story," he said, "so I do not think there is much new news here."
Even those more familiar with the research remain skeptical. "One of the things we see a lot in science is relationships - two things happening together," says Bill Thies, Ph.D., chief medical and scientific officer at the Alzheimer's Association. "But they often turn out to be independent events, or you can't tell which thing is causing which. It could be, for example, that there's something about amyloids that attracts HSV."
Wozniak says that the study he published with Itzhaki - in which the herpes virus caused amyloid accumulation in cells and mice - refutes that criticism. He also dismisses another critique - that he and Itzhaki haven't established the mechanism by which HSV-1 brings about that accumulation. Again, he argues, this study indicates an increase in the enzymes that are responsible for forming amyloid from its precursor protein, called APP.
"Surely, the mechanism is clear: HSV-1 causes an increase in these enzymes, which in turn causes degradation of APP, leading to amyloid formation." He pauses, and then adds wryly, "It's interesting that people raise this criticism when, until our research, no other underlying causes of amyloid production linked to Alzheimer's disease were known."
Itzhaki is more sanguine about the skepticism. "We've seen this before when a virus or bacterium is suggested as the cause for a chronic illness," she says, noting the reticence people had when H. pylori was suggested as a cause of ulcers and when the human papilloma virus was suspected as a cause of cervical cancer. Both are now largely considered medical fact. "And the Alzheimer's establishment is very conservative."
Georgetown's Dr. Federoff agrees that in some ways the theory isn't conventional enough to be embraced by many mainstream Alzheimer's researchers. "Herpes is a common virus, but in this case we're talking about it behaving in an atypical way," he notes. That said, would he like to see further research on the connection between HSV and Alzheimer's? Absolutely.
There is one matter on which the opposing camps agree: With each passing day, the stakes for Alzheimer's research grow higher. Over the past century, the only thing that has prevented the disease from becoming even more widespread and devastating is that most people passed away from something else before they were old enough to develop it.
Drop dead of a heart attack when you're 52, and Alzheimer's is one malady you probably won't have to worry about. (Actually, your biggest health worries are probably less of a risk than you think. But you should watch out for these six threats.) But the more progress we make against our most common killers - heart disease, stroke, and cancer - and the more we extend our life spans, the greater the number of Alzheimer's cases we're likely to see. Indeed, as the 33-million-plus-strong baby boom generation enters its golden years and sees its risk of Alzheimer's increase, we are potentially looking at an epidemic. By 2010, the number of cases is expected to have increased 10 percent from its 2000 total, and from there the number is projected to more than double - to more than 950,000 new cases a year - by 2050.
"Alzheimer's has always been a big problem, but it's going to be even bigger," says Thies. "And the people who are now in their 20s, 30s, and 40s are the ones it's especially going to affect."
So what do you do if you're part of that group - especially if you tend to develop cold sores? One future option could be to have yourself tested for the APOE e4 gene - though Wozniak isn't a fan of that idea. "It would just cause a lot of worry for the person involved and his or her family."
Another possibility might be to take an oral antiviral drug preventively - essentially, to attempt to keep the herpes virus in check before it can do any damage to your brain. The hitch here, however, is that no clinical trials have ever evaluated the safety of taking a daily antiviral, such as Valtrex, for longer than a year. Plus, the average physician would consider the link to Alzheimer's too tenuous to let you play guinea pig.
In the end, the best option may simply be to wait, and hope. When I ask Wozniak whether he and Itzhaki feel like they're running out of time, he says, "Of course. We are all getting older. Our parents are getting older. Soon we'll all be affected one way or another by Alzheimer's disease... if we haven't already."
But too much may do just the opposite, research shows
NEW YORK - Having one or two alcoholic drinks per day may help prevent dementia in the elderly, according to study findings presented Monday at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease in Vienna, Austria. Too much alcohol use, however, may promote dementia.
The results indicate that cognitively normal adults, 75 years or older, who are moderate drinkers are 40 percent less likely to develop dementia over 6 years than are their non-drinking peers. By contrast, alcohol use appears to offer no benefit, and possibly harm, for adults who already have some degree of cognitive impairment.
"We were pleased to see that the beneficial effects of moderate alcohol intake reported in middle-aged adults also extend to cognitively normal older adults over 75," lead author Dr. Kaycee M. Sink, from Wake Forest University School of Medicine in Winston-Salem, North Carolina, told Reuters Health.
Dr. Sink noted that her team's study is not the first to look at the association between alcohol use and the risk of dementia, but said that several factors make it unique.
"It is one of largest, longest studies of older adults living in the U.S. to examine this question; the participants are older than most previously studied; and we were able to look at the effects of alcohol consumption in both cognitively normal older adults as well as those who had mild cognitive impairment."
The subjects included 3,069 adults who were enrolled in the Ginkgo Evaluation of Memory Study (GEMS). Based on extensive testing, the subjects were classified as having normal cognition or mild impairment at baseline. Alcohol use was categorized as none, light, moderate, or heavy, based on having 0, 1 to 7, 8 to 14, or more than 14 drinks per week, respectively.
At the start of the study, 2,587 subjects had normal cognition and 482 had mild cognitive impairment. In terms of alcohol use, about 40 percent were either none or light drinkers, and about 10 percent each were moderate or heavy users.
More than 500 cases of dementia developed in the entire group over the period of the study. As noted, among those who were cognitively normal at the start of the study, moderate alcohol drinkers appeared to be protected against dementia.
In subjects with mild cognitive impairment, however, heavy alcohol users half nearly doubled the risk of dementia relative to non-use, Dr. Sink said.
"Since every individual has different medical conditions and family history, alcohol consumption may not be appropriate for everyone wanting to limit their risk of developing dementia," Dr. Sink noted. "What we can say, based on this study, is that our results support current guideline recommendations for alcohol intake into old age and do not necessarily support the need for people with normal cognition who drink moderately to change their drinking habits."
Long sleepers' show higher dementia risk
Spending 9 or more hours in bed linked to possible mental decline
How could something that feels so good - a long night's sleep - have negative consequences? Unfortunately, that is one possibility that results of a new study suggest: Older adults who sleep nine or more hours each day may have a higher risk of developing dementia than those who spend fewer hours in bed.
Spanish researchers found that among nearly 3,300 older adults they followed for three years, those who slept nine or more hours per day, daytime naps included, were about twice as likely to develop dementia as those who typically slept for seven hours.
These "long sleepers" were at increased risk even when the researchers accounted for several factors that can affect both sleep and dementia risk - including age, education, and smoking and drinking habits.
Still, the findings show only an association between longer sleep and dementia, and do not prove that extra hours in bed, per se, contribute to mental decline.
"It remains to be established how the relation between longer sleep duration and dementia is mediated," Dr. Julian Benito-Leon, of University Hospital '12 de Octubre' in Madrid, told Reuters Health in an email.
One possibility, according to Benito-Leon, is that increased fatigue and sleep is an initial sign of early dementia in some people.
Another theory is that one or more underlying health problems may increase older adults' need for sleep, as well as contribute to dementia. The breathing disorder sleep apnea, for instance, causes fatigue and has been linked to impairments in thinking and memory in older adults.
It's also possible, Benito-Leon said, that excessive sleep somehow directly affects dementia risk - though, if that is true, there is no known physiological explanation.
The study findings, which appear in the European Journal of Neurology, are based on evaluations of 3,286 adults age 65 and older. At the outset, all were screened for dementia and reported on their typical sleep habits.
Over the next three years, 140 study participants were diagnosed with dementia. Among those who had said they slept at least nine hours per day, just over 5 percent developed dementia. That compared with roughly 2 percent of men and women who slept for seven hours per day, and 4 percent of those who logged eight hours.
On the other end of the spectrum, 5 percent of "short sleepers" - those who got five or fewer hours of sleep per day - were diagnosed with dementia during the study. However, when the researchers weighed other factors, lack of sleep, in and of itself, was no longer linked to a higher dementia risk.
While excessive sleep may or may not contribute to dementia, it could be considered a potential sign of a problem, according to Benito-Leon.
He recommended that if an older adult who has typically slept the standard seven or eight hours per day suddenly starts needing more sleep, he or she should discuss the change with a doctor.
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