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.

See the original article here.

The brain’s ability to learn and form memories of day-to-day facts and events depends on the hippocampus, a structure deep within the brain. But is the hippocampus still maintaining the memory of, say, the commencement address at your college graduation 20 years ago? The latest evidence suggests that as memories age, the hippocampus’s participation wanes.

In a 2006 study, neuroscientist Larry R. Squire of the University of California, San Diego, and the Veterans Affairs San Diego Healthcare System studied patients who had hippocampal damage. These indi­viduals did not remember details of newsworthy events that occurred in the five to 10 years prior to their injuries, but they did recall older events.

Building on those results, Squire turned to healthy brains. His team questioned 15 people in their 50s and 60s about events in the news over the past 30 years while scanning the participants’ brains with functional MRI. To single out brain activity related to the date of the event, the researchers separately evaluated activity tied to learning and remem­bering the test questions. They also accounted for the richness of participants’ recollections of events, to make sure the degree to which someone was able to recall an event did not influence the data.

Squire’s team reported in January that activity in the hippocampus steadily declined as subjects remembered events that were up to 12 years old. With more remote memories, the structure’s activity leveled off. In contrast, areas in the frontal, temporal and parietal lobes displayed increasing activity for recalled events from those dozen years, then reached a plateau during older remembrances.

The biology behind how the brain makes and keeps memories is not fully understood, Squire notes, but it appears that, initially, a memory resides in the hippocampus and in areas the structure connects to in the neocortex, the outer part of the cerebral cortex. “A time comes when the cortical regions important to a memory are connected [to one another] heavily enough to form a stable representation,” Squire says. “Then the hippocampus isn’t needed to hold the whole thing together.”

Original article here

Myfitbrain brain games

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

July 20, 2009
BY BRAD SPIRRISON chicagotechmatters@gmail.com

While popular exercise-focused video games like those played on Nintendo’s Wii Fitness appear to have some health benefits, brain games designed to enhance mental fitness are striving for clinical and commercial acceptance.

“We are learning that people can push out the natural effects of aging by playing cognitive games,” says Jim Hanekamp, founder of Glenview-based My Fit Brain.

Hanekamp, 53, started the company last year after his mother began to show early signs of Alzheimer’s. His research showed that while brain exercises could do little to reverse the effects of Alzheimer’s, they could positively impact neural growth earlier in life. This, in theory, could delay memory loss and other effects of brain aging.

The former corporate technology director has invested about $70,000 and months of salary-free time to develop a suite of brain training games found at www.myfitbrain.com. Games with titles like “Pair Em Up” and “CodeBreaker” test memory and logic function, and increase in difficulty based on the cognitive capacity of the user.

While Nintendo and neuroscience specialist Lumosity market paid and subscription-based games, everything on My Fit Brain is free to the user. Hanekamp, who has recruited 1,200 registered users and thousands more visitors to the site, hopes eventually to make money from advertisers.

“We have a new, patent-pending way to incorporate advertising within the game itself,” he said.

Although Hanekamp has had a tough go landing advertisers and investors — he was told he needs between 10,000 and 100,000 registered users to be a viable marketing channel — the company has contained costs by outsourcing its development to India and hosting the site on Amazon’s cloud computing service.

My Fit Brain is marketed largely via word-of-mouth, fueled by an instructive and regularly updated blog on the site that focuses on cognitive fitness issues.

Chicago Sun-Times article by Brad Spirrison

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.

By uncovering a mechanism that causes damage to brain synapses during Alzheimer’s disease, researchers might have found a key to reducing or preventing nerve degeneration for these patients.

According to a report in the April 3 issue of Science, researchers at the U.S.-based Burnham Institute for Medical Research have shown that beta-amyloid protein “multimers” create excessive nitric oxide. This free radical then reacts with the protein Drp1, causing the fragmentation of mitochondria — the cell’s energy storehouses — in the brain, a violent process that causes the neurodegeneration linked to Alzheimer’s disease.

Finish reading this article at: Brain Cells Give New Clues

When is a memory lapse just a lapse and when is it a sign of something much more serious? Loss of memory is a great fear among older adults. Our memories define us.

According to the Alzheimer’s Association, every 71 seconds someone develops Alzheimer’s and 10 million baby boomers will develop Alzheimer’s disease in their lifetime.

All of us over a certain age have probably experienced a few “senior moments” — those disconcerting memory blips when you can’t come up with the right word, remember where you put the remote or even remember why you walked into a room. When we are younger, we can laugh off these memory lapses, but as we age they can become worrisome.

In the same way people have worked to reduce their risk of cardiovascular disease through diet and exercise, people can work to improve the health of their brains. Brain fitness can delay and even help reclaim some age-related cognitive decline and memory loss. Studies have shown it is not just a case of “use it or lose it.” With the right stimulation, it’s more like “use it and boost it.”
The article continues by explaining ways for individuals to stimulate their brain cells. If you are interested in learning about this, click the following link: Focus on Aging Brain