The idea that the adult brain changes with experience was once a radical idea, but it is now well accepted that certain areas—say, the motor cortex, when learning a new physical skill—can grow new neurons or create stronger connections.

Now scientists report that the brain is even more mutable than suspected. Thanks to an unconventional research technique, neuroscientists have found the first physical proof that new experiences and information have wide-ranging effects throughout both hemispheres of the brain, rather than just creating connections in one discrete area.

“We have learned that what we call neuronal plasticity isn’t exclusive to individual synapses or even the neurons where they contact but rather occurs throughout the functional network in which synapses and neurons are embedded,” Canals says. “Those networks are absent in brain slices, so they couldn’t be studied before.”

By showing how activity in the hippocampus causes widespread changes in brain structure, Canals says the findings could explain why new memories are at first dependent on the hippocampus but can eventually be recalled without triggering that part of the brain at all.

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Generate new neurons by playing brain games at 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

Professor Elizabeth Gould received the  prestigious Benjamin Franklin from the RSA organization for her groundbreaking work on neurogenesis. Her research into the effect of environments on the neuronal composition of the brain has profound and far-reaching societal implications.

Good video on how neurogenesis works in the hippocampus and why working out your brain helps it to improve for the long run.  Also how anxiety can inhibit neurogenesis which inhibits your ability to learn.

The human brain can adapt to changing demands even in adulthood, but MIT neuroscientists have now found evidence of it changing with unsuspected speed. Their findings suggest that the brain has a network of silent connections that underlie its plasticity.

The brain’s tendency to call upon these connections could help explain the curious phenomenon of “referred sensations,” in which a person with an amputated arm “feels” sensations in the missing limb when he or she is touched on the face. Scientists believe this happens because the part of the brain that normally receives input from the arm begins “referring” to signals coming from a nearby brain region that receives information from the face.

“We found these referred sensations in the visual cortex, too,” said senior author Nancy Kanwisher of the McGovern Institute for Brain Research at MIT, referring to the findings of a paper being published in the July 15 issue of the Journal of Neuroscience. “When we temporarily deprived part of the visual cortex from receiving input, subjects reported seeing squares distorted as rectangles. We were surprised to find these referred visual sensations happening as fast as we could measure, within two seconds.”

Many scientists think that this kind of reorganized response to sensory information reflects a rewiring in the brain, or a growth of new connections.

“But these distortions happened too quickly to result from structural changes in the cortex,” Kanwisher explained. “So we think the connections were already there but were silent, and that the brain is constantly recalibrating the connections through short-term plasticity mechanisms.”

First author Daniel Dilks, a postdoctoral researcher in Kanwisher’s lab, first found the square-to-rectangle distortion in a patient who suffered a stroke that deprived a portion of his visual cortex from receiving input. The stroke created a blind region in his field of vision. When a square object was placed outside this blind region, the patient perceived it as a rectangle stretching into the blind area – a result of the the deprived neurons now responding to a neighboring part of the visual field.

“But the patient’s cortex had been deprived of visual information for a long time, so we did not know how quickly the adult visual cortex could change following deprivation,” Dilks said. “To find out, we took advantage of the natural blind spot in each eye, using a simple perceptual test in healthy volunteers with normal vision.”

Blind spots occur because the retina has no photoreceptors where the optic nerve exits the eye, so the visual cortex receives no stimulation from that point. We do not perceive our blind spots because the left eye sees what is in the right eye’s blind area, and vice versa. Even when one eye is closed, we are not normally aware of a gap in our visual field.

It takes a perceptual test to reveal the blind spot, which involves covering one eye and moving an object towards the blind spot until it “disappears” from view.

Dilks and colleagues used this test to see how soon after the cortex is deprived of information that volunteers begin to perceive shape distortions. They presented different-sized rectangles just outside the subjects’ blind spot and asked subjects to judge the height and width at different time points after one eye was patched.

The volunteers perceived the rectangles elongating just two seconds after their eye was covered – much quicker than expected. When the eye patch was removed, the distortions vanished just as fast as they had appeared.

“So the visual cortex changes its response almost immediately to sensory deprivation and to new input,” Kanwisher explained. “Our study shows the stunning ability of the brain to adapt to moment-to-moment changes in experience even in adulthood.”

Notes:

Chris Baker (NIH) and Yicong Liu (MIT undergraduate student) contributed to this study, which was supported by the NIH and NIMH.

Written by Cathryn Delude, McGovern Institute, MIT News Office

Researchers have shown for the first time that neural stem cells can rescue memory in mice with advanced Alzheimer’s disease, raising hopes of a potential treatment for the leading cause of elderly dementia that afflicts 5.3 million people in the U.S.

Dementia is a general term for a group of brain disorders that affect memory, judgment, personality and other mental functions. Alzheimer’s is the most common type of dementia, accounting for 60 to 80 percent of cases. There is currently no cure for Alzheimer’s.

Modified Alzheimer’s mice performed markedly better on memory tests a month after mouse neural stem cells were injected into their brains. The stem cells secreted a protein that created more neural connections, improving cognitive function.

“Essentially, the cells were producing fertilizer for the brain,” said Frank LaFerla, co-author of the study.

Lead author Mathew Blurton-Jones and colleagues worked with older mice predisposed to develop brains lesions called plaques and tangles that are the hallmarks of Alzheimer’s.

To learn how the stem cells worked, the scientists examined the mouse brains. To their surprise, they discovered that just 6 percent of the stem cells had turned into neurons. (The majority became the other two main types of brain cells, astrocytes and oligodendrocytes.) The stem cells didn’t improve cognition by becoming new neurons, nor did they act by reducing the number of plaques and tangles.

Rather, the stem cells were found to have secreted a protein called brain-derived neurotrophic factor, or BDNF. This caused existing tissue to sprout new neurites, strengthening and increasing the number of connections between neurons. When the team selectively reduced BDNF from the stem cells, the benefit was lost, providing strong evidence that BDNF is critical to the effect of stem cells on memory and neuronal function.

“If you look at Alzheimer’s, it’s not the plaques and tangles that correlate best with dementia; it’s the loss of synapses, connections between neurons,” Blurton-Jones said. “The neural stem cells were helping the brain form new synapses and nursing the injured neurons back to health.”

Diseased mice injected directly with BDNF also improved cognitively but not as much as with the neural stem cells, which provided a more long-term and consistent supply of the protein.

“This gives us a lot of hope that stem cells or a product from them, such as BDNF, will be a useful treatment for Alzheimer’s,” LaFerla said.

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ATLANTA — Researchers at Georgia State University have found that diets high in fructose — a type of sugar found in most processed foods and beverages — impaired the spatial memory of adult rats.

Amy Ross, a graduate student in the lab of Marise Parent, associate professor at Georgia State’s Neuroscience Institute and Department of Psychology, fed a group of Sprague-Dawley rats a diet where fructose represented 60 percent of calories ingested during the day.

She placed the rats in a pool of water to test their ability to learn to find a submerged platform, which allowed them to get out of the water. She then returned them to the pool two days later with no platform present to see if the rats could remember to swim to the platform’s location.

“What we discovered is that the fructose diet doesn’t affect their ability to learn,” Parent said. “But they can’t seem to remember as well where the platform was when you take it away. They swam more randomly than rats fed a control diet.”

Fructose, unlike another sugar, glucose, is processed almost solely by the liver, and produces an excessive amount of triglycerides — fat which get into the bloodstream. Triglycerides can interfere with insulin signaling in the brain, which plays a major role in brain cell survival and plasticity, or the ability for the brain to change based on new experiences.

Results were similar in adolescent rats, but it is unclear whether the effects of high fructose consumption are permanent, she said.

Parent’s lab works with Timothy Bartness, Regents’ Professor of Biology, and John Mielke of the University of Waterloo in Waterloo, Ontario, Canada to examine how diet influences brain function.

Although humans do not eat fructose in levels as high as rats in the experiments, the consumption of foods sweetened with fructose — which includes both common table sugar, fruit juice concentrates, as well as the much-maligned high fructose corn syrup — has been increasing steadily. High intake of fructose is associated with numerous health problems, including insulin insensitivity, type II diabetes, obesity and cardiovascular disease.

“The bottom line is that we were meant to have an apple a day as our source of fructose,” Parent said. “And now, we have fructose in almost everything.” Moderation is key, as well as exercise, she said.

Exercise is a next step in ongoing research, and Parent’s team will investigate whether exercise might mitigate the memory effects of high fructose intake. Her lab is also researching whether the intake of fish oil can prevent the increase of triglycerides and memory deficits. Results from that research will be presented by her graduate student Emily Bruggeman at the 2009 Society for Neuroscience meeting in Chicago this fall.

Training increases brain processing speed and improves our ability to multitask, new research from Vanderbilt University published in the June 15 issue of Neuron indicates.

“We found that a key limitation to efficient multitasking is the speed with which our prefrontal cortex processes information, and that this speed can be drastically increased through training and practice,” Paul E. Dux, a former research fellow at Vanderbilt, and now a faculty member at the University of Queensland in Brisbane, Australia, and co-author of the study, said. “Specifically, we found that with training, the ‘thinking’ regions of our brain become very fast at doing each task, thereby quickly freeing them up to take on other tasks.”

To understand what was occurring in the brain when multitasking efficiency improved, the researchers trained seven people daily for two weeks on two simple tasks — selecting an appropriate finger response to different images, and selecting an appropriate vocal response (syllables) to the presentation of different sounds. The tasks were done either separately or together (multitasking situation). Scans of the individuals’ brains were conducted three times over the two weeks using functional magnetic resonance imaging (fMRI) while they were performing the tasks.

Before practice, the participants showed strong dual-task interference—slowing down of one or both tasks when they attempted to perform them together. As a result of practice and training, however, the individuals became very quick not only at doing each of the two tasks separately, but also at doing them together. In other words, they became very efficient multitaskers.

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