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A Bigger Brain May Help Protect You from Alzheimer’s

While nobody can control the size of their brains, experts advise that mentally stimulating activities like completing puzzles, traveling, learning a new language, playing a musical instrument, or doing crossword puzzles can help stimulate new connections between brain cells.



A Bigger Brain May Help Protect You from Alzheimer’s

A large hippocampus – a part of the brain devoted to memory – may help ward off Alzheimer’s disease, a new study reports. The findings offer new clues into why some elderly people remain mentally sharp and alert well into their 80s and beyond, even though their brains are riddled with the plaques and tangles of Alzheimer’s disease.

The findings help support the notion of cognitive reserve, the theory that a brain rich in interconnections and working nerve cells may help to ward off the symptoms of Alzheimer’s disease even when a certain amount of brain tissue is already damaged. With a larger hippocampus, the more brain cells. According to the theory, if some cells die off from the ravages of Alzheimer’s or related ailments, enough cells remain so that people can continue to think and function normally..

From autopsies, researchers have long known that some people die with sharp minds and perfect memories, even though their brains are riddled with the plaques and tangles of Alzheimer’s disease. The new research suggests that people who have a larger hippocampus, a seahorse-shaped part of the brain that is critical for memory, may as a result be protected against Alzheimer’s.

“This larger hippocampus may protect these people from the effects of Alzheimer’s disease-related brain changes,” said study author Deniz Erten-Lyons, M.D., with Oregon Health & Science University in Portland. “Hopefully this will lead us eventually to prevention strategies.”

For the study, presented April 15 at the American Academy of Neurology 60th Annual Meeting in Chicago, researchers evaluated the brains of 12 people who had sharp memories and thinking skills at the time of their death. Autopsies revealed that their brains contained large numbers of Alzheimer’s plaques, even though they remained mentally sharp and alert. Their brains were compared to those of 23 people who had the same amount of plaques in their brains, but had been diagnosed with Alzheimer’s disease before death.

Researchers found that the volume of the hippocampus area of the brain was 20 percent larger in the cognitively intact group compared to the Alzheimer’s disease group with dementia. There were no other demographic, clinical or pathological differences between the groups. The results remained the same regardless of whether they were men or women, their age and the total brain volume.

The findings help to explain why many people remain mentally sharp well into their 80s and beyond, even though autopsies after death show that their brains contain extensive damage like that seen in Alzheimer’s disease.

While nobody can control the size of their brains, experts advise that mentally stimulating activities like completing puzzles, traveling, learning a new language, playing a musical instrument, or doing crossword puzzles can help stimulate new connections between brain cells. These strengthened connections may help to preserve thinking and memory. Maintaining strong social ties and exercising into old age may also help to protect the brain, studies show.

To learn more about keeping the brain young, visit http://www.ALZinfo.org, The Alzheimer’s Information Site.

By alzinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.
Source: Presented at the American Academy of Neurology 60th Anniversary Annual Meeting in Chicago, April 12 to 19, 2008.

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Silent Seizures May Cause Alzheimer’s Dementia

The surprising finding indicates that antiseizure medications given to epilepsy patients may also help lower or even reverse cognitive decline in Alzheimer’s disease, a treatment option that could be available relatively quickly.

Source Scientific America

Study identifies nonconvulsive seizures as potential culprit. Already available drugs may stave off and even reverse debilitating symptoms

By Nikhil Swaminathan

The families of the five million Alzheimer’s disease sufferers in the U.S. are all too familiar with the erratic neurodegenerative disorder. “Mom seemed almost like herself this morning and then she drifted away form me,” recounts senior investigator Lennart Mucke, describing a conversation with a patient’s daughters.
The root of these heart-wrenching fluctuations between cognizance and confusion has eluded scientists for years. But Mucke, director of the Gladstone Institute of Neurological Disease at the University of California, San Francisco, and colleagues believe they may finally have pinpointed the cause of these puzzling personality twists as well as other cognitive deficits associated with Alzheimer’s: petite mal (nonconvulsive) seizures similar to those exhibited in some types of epilepsy.

They reached this conclusion during studies of mice engineered to build up protein fragments in their brains known to cause the disease. The animals had alternating stages of overexcitement and inhibition in several regions of their brains, seizures of activity that resulted in swift rewiring to dampen the sudden surges.
“We were quite struck to find anatomical and pathological hallmarks of overexcitation” observed in epilepsy without the convulsive, physical reaction, says Mucke. “We would have thought that everything was shutting off.”

The surprising finding indicates that antiseizure medications given to epilepsy patients may also help lower or even reverse cognitive decline in Alzheimer’s disease, a treatment option that could be available relatively quickly.

A protein fragment called amyloid-beta (Aβ) is known to aggregate and create plaque in the brains of Alzheimer’s patients. Plaque hinders neuronal activity by gumming up synapses (spaces between cells through which chemical or electrical information is transmitted), eventually damaging nerve cell branches and leading to neuronal death.

In the current study, a collaborative team of researchers at the Gladstone Institute and the Baylor College of Medicine in Houston, created a strain of mice that overproduces a precursor of Aβ known as amyloid precursor protein. Five to six months after birth, as plaque built up, these animals showed learning and memory deficits illustrated by their difficulty navigating mazes. During autopsies, researchers observed that rewiring had occurred in the late subjects’ brains.

“What tipped us off to the excitation was actual anatomical rewiring in the hippocampus—or learning centers—that looked like the cells wanted to protect themselves from overexcitation,” Mucke says.

Using electroencephalography (EEG)—in which electrodes placed in the brain measure neural activity—the team saw a sharp wave of action in the mouse brains from the hippocampus in the midbrain to the neocortex (the outermost brain layer). The whole network of nerve cells seemed to activate simultaneously and synchronously. “The hippocampus then clamps down because it doesn’t want to receive all that excitation, so it clamps down its portals by engaging its inhibitory cells,” Mucke says. “In the process, they probably disable some normal, excitatory functions; part of this inhibitory rewiring that happens probably accounts for the fact that there’s no physical seizure activity.”

He says it is no doubt difficult for the neurons to do their usual jobs in the face of the sudden bursts of activity and overcompensation to correct them. Given that the hippocampus is associated with episodic memory, he says that this may account for some of the cognitive deficits of Alzheimer’s, including the spells of confusion. “I could imagine that this abnormal activity may go on throughout the course of the disease,” Mucke notes, “and not just mess up cognition but contribute to the neurodegenerative process.”

The 36-Hour Day: A Family Guide to Caring for People with Alzheimer Disease and Memory Loss in Later Life

 

Scientists find early signs of Alzheimer’s

“We found the earliest predictor,” said the lead researcher, Lisa Mosconi of New York University School of Medicine. “The hippocampus seems to be the very first region to be affected.”

Source USA Today

A subtle change in a memory-making brain region seems to predict who will get Alzheimer’s disease nine years before symptoms appear, scientists reported Sunday.
The finding is part of a wave of research aimed at early detection of the deadly dementia — and one day perhaps even preventing it. (Related: Lifestyle, Alzheimer’s link strengthen Disease explained)

Researchers scanned the brains of middle-aged and older people while they were still healthy. They discovered that lower energy usage in a part of the brain called the hippocampus correctly signaled who would get Alzheimer’s or a related memory impairment 85% of the time.

“We found the earliest predictor,” said the lead researcher, Lisa Mosconi of New York University School of Medicine. “The hippocampus seems to be the very first region to be affected.”

But it is too soon to offer Alzheimer’s-predicting PET scans. The discovery must be confirmed. Also, there are serious ethical questions about how soon people should know that Alzheimer’s is approaching when nothing yet can be done to forestall the disease.

Still, the discovery may provide leads to scientists searching for therapies to at least delay the onset of the degenerative brain disease. It already affects 4.5 million people in the U.S. and is predicted to strike 14 million by 2050 as the population ages.

Moreover, researchers are honing in on lifestyle choices that may help protect the brain in the first place.

“It’s exciting that we can even talk about prevention,” said William Thies, scientific director of the Alzheimer’s Association. He noted that just 10 years ago there was hardly any research into that possibility.

Among the findings presented Sunday at the association’s first Alzheimer’s prevention conference:

•People who drink fruit or vegetable juice at least three times a week seem four times less likely to develop Alzheimer’s than nonjuice drinkers, according to a study of 1,800 elderly Japanese-Americans. The theory is that juice contains high levels of polyphenols, compounds that may play a brain-protective role.

•Less education, gum disease early in life, or a stroke were more important than genes in determining who got dementia, concluded a study of 100 dementia patients with healthy identical twins. Education stimulates neuronal growth; gum disease is a marker of brain-harming inflammation.

•Decreasing social activity in old age is a risk factor, a National Institute on Aging study suggests. It is not clear if the men in the study became less social because Alzheimer’s already was at work, but social activity is mentally stimulating.

A brain-healthy lifestyle aside, a big quest is to develop ways to identify Alzheimer’s disease before symptoms emerge — finding biomarkers that could be targets for preventive therapies.

Think of it as hunting the equivalent of the cholesterol test for Alzheimer’s, Dr. Neill Graff-Radford of the Mayo Clinic said.

He measured blood levels of different types of beta amyloid, the sticky protein that makes up Alzheimer’s hallmark brain plaques, in 565 people. Those with lowest ratios of a particular amyloid type were three times more likely to develop dementia within five years.

The reason: Probably less amyloid was floating in the blood because it was sticking in the brain instead.

PET scans already can show Alzheimer’s plaques in advanced disease. Mosconi’s study is the first to so rigorously examine people’s brains before symptoms appear.

PET, or positron emission tomography, scans show images of how brains use glucose, or sugar, which is the brain’s main fuel.

Mosconi scanned 53 healthy people. She tracked them for up to 24 years. Six so far have developed Alzheimer’s and 19 developed an Alzheimer’s precursor called “mild cognitive impairment,” or MCI. Those people showed less glucose metabolism in the hippocampus than the still healthy.

Other research supports the hippocampus’ early role.

University of Wisconsin researchers gave a different brain scan, called a functional MRI, to healthy adult children of Alzheimer’s patients. The researchers found that the hippocampus was not as active as in people without that familial risk.

To prove if these early indicators are real, the National Institute on Aging, with financial help from the pharmaceutical industry and Alzheimer’s Association, is beginning a $60 million study to scan the brains of 800 older Americans and try to pin down Alzheimer’s earliest biological changes.

That Alzheimer’s begins developing so early means even young people should adopt a brain-healthy lifestyle, said Dr. Mark Sager of the Wisconsin Registry for Alzheimer’s Prevention. “what we’re hoping is that 55 is not too late,” he said.

 
 
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