Persons with higher levels of leptin, a protein hormone produced by fat cells and involved in the regulation of appetite, may have an associated reduced incidence of Alzheimer disease and dementia, according to a study in the December 16 issue of JAMA.

Previous studies have shown that overweight and obesity in mid-life are associated with poorer cognitive function in the general population and an increased risk of dementia. There has been evidence that leptin exerts additional functions on the brain outside the hypothalamus (a region of the brain that controls body temperature, hunger, and thirst), according to background information in the article.

The researchers found that higher leptin levels were associated with a lower incidence of  dementia and AD. The incidence of dementia decreased gradually across increasing levels of leptin: a person with a baseline leptin level in the lowest quartile group had a 25 percent risk of developing AD after 12 years of follow-up, whereas the corresponding risk for a person in the top quartile group was only 6 percent.

“These findings are consistent with recent experimental data indicating that leptin improves memory function in animals through direct effects on the hippocampus and strengthens the evidence that leptin is a hormone with a broad set of actions in the central nervous system. Due to the exploratory character of the present analyses, we did not adjust for multiple comparisons and acknowledge that our findings require confirmation in independent samples,” the authors write.

“If our findings are confirmed by others, leptin levels in older adults may serve as one of several possible biomarkers for healthy brain aging and, more importantly, may open new pathways for possible preventive and therapeutic intervention. Further exploration of the molecular and cellular basis for the observed association may expand our understanding of the pathophysiology underlying brain aging and the development of AD.”
(JAMA 2009;302[23]:2565-2572. )

Seniors may be able to slow down memory loss by exercising the brain, experts say.

Doing crossword puzzles, playing cards and other games might ward off a decline in memory or help us maintain “brainpower” as we age, reports a study by the Rush Alzheimer’s Disease Center and Rush-Presbyterian-St. Luke’s Medical Center in Chicago. The study found that more frequent participation in cognitively stimulating activities is associated with a reduced risk of Alzheimer’s Disease.

The research looked at everyday activities such as reading books, newspapers or magazines, engaging in crossword puzzles or card games, and going to museums among aging participants. The 2002 study followed more than 700 dementia-free participants age 65 and older for an average of 4.5 years. The results indicated a one-point increase in cognitive activity corresponded with a 33 percent reduction in the risk of Alzheimer’s.

“The brain is like a muscle. If you don’t use it, you lose it,” said Jim Hanekamp, founder of Glenview-based Web site www.myfitbrain.com. The Web site features a variety of cognitive games that are geared to exercising the mind.

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When inflammation arises in the body as a result of infection or injury, the immune response also appears to accelerate memory loss in people with Alzheimer’s, according to a recent study published in the journal Neurology. In this study of changes in patients’ cognitive abilities over a span of six months, Alzheimer’s patients who had chronic (ongoing) inflammation as a result of, for instance, obesity or arthritis experienced four times the amount of memory loss as compared with patients without such inflammation. And those with chronic inflammation who also experienced an acute immune response (short-term, such as from an infection) were even worse off: their memory loss accelerated 10 times faster than patients without any inflammation.

“When we started the study, we thought short-lived events would be impor­tant,” says lead author Clive Holmes, a professor of biological psychiatry at the University of Southampton in England. “We hadn’t realized how important chronic inflammation was going to be.”

So how does inflammation, whether from an infection or from chronic dis­ease, damage the brain? The answer lies in the body’s immune response, which launches an attack on invading pathogens, releasing inflaming proteins such as tumor necrosis factor, or TNF. This molecule causes the vagus nerve, which extends from the brain to the abdomen and controls vital functions such as heartbeat, to send an electrical im­pulse to the brain, thereby directing the brain to secrete its own immune messengers.

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Cell phone exposure may be helpful in the fight against Alzheimer’s disease, a new study shows.

The study, involving mice, provides evidence that long-term exposure to electromagnetic waves associated with cell phone use may protect against, and even reverse, Alzheimer’s disease.

The study is published in the Journal of Alzheimer’s Disease.

“It surprised us to find that cell phone exposure, begun in early adulthood, protects the memory of mice otherwise destined to develop Alzheimer’s symptoms,” study researcher Gary Arendash, PhD, of the University of South Florida, says in a news release. “It was even more astonishing that the electromagnetic waves generated by cell phones actually reversed memory impairment in old Alzheimer’s mice.”

The researchers say they found that exposing old mice with Alzheimer’s disease to electromagnetic waves generated by cell phones reduced brain deposits of beta-amyloid. Brain plaques formed by the abnormal accumulation of beta-amyloid are hallmarks of Alzheimer’s disease, which is why most treatments try to target the protein.

The study involved 96 mice, including mice genetically engineered to develop Alzheimer’s disease and normal mice. Both the Alzheimer’s mice and the normal rodents were exposed to the electromagnetic field generated by standard cell use for two one-hour periods daily for seven to nine months.

The researchers say that if cell phone exposure was begun when the Alzheimer’s mice were young adults, and before signs of memory loss became apparent, their cognitive ability was protected. And if older mice with Alzheimer’s were exposed, their memory impairment improved. What’s more, months of cell phone exposure even boosted the memories of normal mice, the researchers write.

The researchers say the memory benefits in normal mice of cell phone exposure took months to show up, suggesting a similar effect in humans might take years. However, they also caution that “care should be taken in extrapolating our results to cell phone use and [electromagnetic wave] exposure in humans.”

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A large, 5-year study showed that the people in their 70s who were the most active and adhered the best to a Mediterranean-style diet were 61–67 percent less likely to develop Alzheimer’s disease compared with the least active and least Mediterranean-minded of the group.

Exercise
The most active in the study group got about an hour and a half of exercise weekly. That’s just a few 30-minute walks a week — a pretty manageable commitment. Better yet, aim to walk 30 minutes every day.

Diet
People with the lowest dementia risk ate the highest amounts of fruit, veggies, legumes, and fish, but less meat and dairy products. Monounsaturated fats, like olive oil, also accounted for more of their fat intake than saturated fats. All very typical ratios in a Mediterranean-style diet that doctors and health experts alike recommend for all sorts of reasons. These nutrient-dense, healthy-fat-focused foods could help protect brains against disease and cognitive decline and help protect the body from lots of other bad things, too.

Understanding exactly how the brain encodes and stores memories is one of the central, unsolved mysteries in neuroscience. Currently the most widely accepted theory is long-term potentiation (LTP)—the lasting communication established between two neurons when they are stimulated simultaneously.

As a person processes an event, two neurons pass information through a small space called a synapse. This chemical conversation triggers an intricate cascade, inviting nearby neurons to fire and ultimately creating a network of connections with varying strengths. Afterward, this pattern of connections, or memory, remains within the network of neurons that processed the event.

Although many areas of the brain contain synapses capable of creating strong patterns of connectivity, the hippocampus is a particularly favorable spot for recording memories. This brain region plays a critical role in learning new information, forming spatial memories and storing short-term memories as long-term ones.

Memories formed with the hippo­campus are especially rich because they integrate input from several areas of the brain, and the ­hippocampus contains densely packed layers of neurons. In addition, damage to this region and nearby areas causes profound and perm­anent amnesia—an inability to store new memories or to recall old ones—and is observed in patients who have Alz­heimer’s disease.

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Learn to create new memories faster by playing Myfitbrain

Researchers at MIT’s Picower Institute for Learning and Memory conducted learning and memory tasks using transgenic mice that were induced to lose a significant number of brain cells. Following Alzheimer’s-like brain atrophy, the mice acted as though they did not remember tasks they had previously learned.  But after taking HDAC inhibitors, the mice regained their long-term memories and ability to learn new tasks. In addition, mice genetically engineered to produce no HDAC2 at all exhibited enhanced memory formation.

The fact that long-term memories can be recovered by elevated histone acetylation supports the idea that apparent memory “loss” is really a reflection of inaccessible memories, Tsai said. “These findings are in line with a phenomenon known as ‘fluctuating memories,’ in which demented patients experience temporary periods of apparent clarity,” she said.

A team led by researchers at MIT’s Picower Institute for Learning and Memory has now pinpointed the exact gene responsible for a 2007 breakthrough in which mice with symptoms of Alzheimer’s disease regained long-term memories and the ability to learn. In the latest development, reported in the May 7 issue of Nature, Li-Huei Tsai, Picower Professor of Neuroscience, and colleagues found that drugs that work on the gene HDAC2 reverse the effects of Alzheimer’s and boost cognitive function in mice.

Original article here