Cognitive Labs

Exercising your mind does pay off - for the first time, scientists have shown that learning slows the build-up in the brain of protein plaques and tangles that are the signature of Alzheimer's disease.

Although the study was conducted in mice, it does reinforce the idea that, in humans, maintaining an active mind may help delay or even prevent Alzheimer's disease.

"This has shown for the first time that using your brain can protect you physically," said Kim Green, co-lead author of the study and a postdoctoral researcher at the University of California, Irvine. "We show that when you do this, it causes changes in the brain, and these changes are protective."

"It's an interesting study, and part of what it does is advance the notion that mental exercise has a protective effect against Alzheimer's," said Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City.

According to the Alzheimer's Association, about 4.5 million Americans have the brain-robbing disorder, a number that has more than doubled since 1980. Many more suffer from cognitive impairment, which could be a harbinger of Alzheimer's.

Many experts believe that Alzheimer's is caused by a steady accumulation of amyloid plaque proteins in the brain.

Previous studies had shown that "mental exercise" could delay the onset of the disease, but the proof came only in the form of memory and other cognitive testing measures.

The study involved hundreds of "transgenic" mice -- mice that had been genetically altered to develop human Alzheimer's disease.

Mice in a "learning" group were allowed to swim in a tank of water until they discovered a submerged platform on which to stand. This training took place four times a day for one week at two, six, nine, 12, 15 and 18 months of age. The other group of mice swam in the tank just once before their learning and memory skills were tested and their brains examined.


Mice up to 1 year old in the learning group developed 60 percent less of the proteins that form plaques and tangles compared to mice in the non-learning group, the researchers found.

"The sort of learning we gave the animals was fairly mild, yet it still had a big effect," Green said.

However, by 15 months of age, the learning mice had declined and were now physically and cognitively identical to the non-learning mice.
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Can these findings be extrapolated to humans?

"We do find a lot of similarities, but clinical data also backs up what we've shown in this study," Green said.

"I think it's reasonable to extrapolate," Kennedy added. "The recommendation certainly is to keep your mind active."

"Think of the brain as a computer," Kennedy continued. "Alzheimer's degrades the hardware, and education enhances the software. The brain is also a muscle, and conditioning may protect it."

Green and his colleagues hope to use the information to one day develop a drug for the disease.

"We want to identify exactly how learning influences pathology and identify a novel drug target," he said.


The study is appearing in the Jan. 24 issue of the Journal of Neuroscience.

Labels: alzheimers, brain, learning, neuroscience, uc-irvine

Key Chemical Impacts Memory, Learning, Retention

The chemical neurotrophin-3 appears to stimulate and encourage growth of interconnecting networks of nerves in the cerebral cortex, according to new research at UC-Irvine. When neurotrophin-3 is absent, growth and connections are less robust. This dichotomy may help to explain memory and cognitive decline seen in Alzheimer's patients - and point toward potential treatments. The research will be revealed in Neuroscience, December 1 issue.

Richard Robertson, professor of anatomy and neurobiology, and other researchers from UCI's School of Medicine found that cholinergic nerve fibers grow toward sources of neurotrophin-3 during early development. In experiments with mice, without neurotrophin-3 to direct growth, the developing cholinergic nerve fibers appeared to not recognize their normal target cells in the brain. Because of this, the axon nerve fibers aided by these circuits grew irregularly and missed their specific target neural cells.

This finding, according to Robertson, has significant implications for neurodegenerative diseases like Alzheimer's. Cholinergic neuronal circuits play a key role in the proper information processing by the cerebral cortex and other areas of the brain. The cerebral cortex is the part of the brain that determines intelligence, personality, and planning and organization, and these actions are compromised by neurodegenerative diseases.

"Studies on the brains of Alzheimer's patients have shown a marked decline in these cholinergic circuits. Our work demonstrates that neurotrophin-3 is essential to maintain the connections to cerebral cortex neurons," Robertson said. "This study shows that a neurotrophin-3 therapy may be able to induce nerve fibers to regrow in the cerebral cortex, which would be beneficial to people with Alzheimer's."

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Labels: alzheimers exercise brain canada, cognitive, cognitive_labs, neurotrophin, uc-irvine