Articles from: 2006 | 2005 | 2002
Recent scientifc findings about the brain and memory:
Researchers today claim to have developed a vaccine that reverses memory loss in Alzheimer's diseased mice. They say it is created from specialized blood cells, has no side effects and needs to be given only occasionally.
Researchers at the Johnnie B. Byrd, Sr. Alzheimer's Center & Research Institute in Tampa, Florida, are making this claim.
In a study published this week in the journal, Neurobiology of Disease, the researchers report that tests of the new vaccine on mice shows promise of reversing memory loss and seriously slowing the effects of Alzheimer's on patients.The groundbreaking research was done by investigators from the Byrd Alzheimer's Institute, the University of South Florida, and University of California Riverside.
In the study, researchers took ordinary white blood cells (immune cells) from normal mice and exposed those white blood cells to an abnormal protein called "beta-amyloid." Beta-amyloid accumulates in Alzheimer's brains and appears to be the root cause of this devastating disease.
A single injection of white blood cells "sensitized" to beta-amyloid was given to Alzheimer's mice with impaired memories and Alzheimer's-like brain pathologies. When the Alzheimer's mice were tested several months later, their memory performance was surprisingly improved, even up to the level of normal mice. Moreover, this single vaccine treatment increased connections between brain cells and reduced brain levels of beta-amyloid in the Alzheimer's mice."This adoptive transfer vaccine approach is important not only for the long-term benefits it provides, but also for what it doesn't provide -- harmful side effects," said Gary Arendash, Ph.D, a principal investigator on the study and a Byrd Institute researcher.
Plans for clinical trials with the new vaccine in Alzheimer's patients are underway at the Byrd Alzheimer's Center and Research Institute. "Even if this new vaccine does not cure Alzheimer's disease, it may significantly slow down the disease process and thus provide years of quality life to individuals diagnosed with the disease," said Arendash.The new vaccine created by Byrd Institute researchers and their collaborators did not induce an inflammatory response in either the blood or brain of Alzheimer's mice, said Dr. Douglas Ethell of the University of California, another principle investigator in the study.
The Byrd Alzheimer's Research Institute is based at the University of South Florida in Tampa, Fl., and is the state's center of excellence for Alzheimer's research. The Byrd Alzheimer's Institute is Florida's only Alzheimer's Disease Research Center, a designation from the National Institutes of Health.
May 23, 2006
UCLA study finds that simple lifestyle changes may improve cognitive function and brain efficiency. May 23, 2006 - A UCLA research study published in the June issue of the American Journal of Geriatric Psychiatry found that people may be able to improve their cognitive function and brain efficiency by making simple lifestyle changes such as incorporating memory exercises, healthy eating, physical fitness and stress reduction into their daily lives.
"We've known for several years that diet and exercise can help people maintain their physical health and live longer, but maintaining mental health is just as important," said lead investigator, Dr. Gary Small, professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA. "The UCLA study is the first to show the impact of memory exercises and stress reduction used together with a healthy diet and physical exercise to improve brain and cognitive function."
Researchers found that after just 14 days of following healthy lifestyle strategies, study participants' brain metabolism decreased in working memory regions, suggesting an increased efficiency - so the brain didn't have to work as hard to accomplish tasks.
For the two-week study, 17 subjects with normal baseline memory performance scores were randomly assigned to two groups: a control group did not make any behavior modifications, while a test group incorporated healthy longevity strategies to improve physical and mental function.
Details of the healthy strategies employed in the study also are highlighted in Small's new book to be published today, "The Longevity Bible: 8 Essential Strategies for Keeping Your Mind Sharp and Your Body Young" (Hyperion, New York, 2006).
Participants on the healthy longevity plan incorporated the following into their daily routine:
- To stimulate the brain, memory exercises such as crossword puzzles and brainteasers were conducted throughout the day.
- To improve physical fitness, participants took daily walks, which have been found to increase life expectancy and lower the risk of Alzheimer disease.
- To improve their diet, study participants on the plan ate five small meals a day, which prevents drops in blood glucose levels since glucose is the main energy source for the brain. In addition, they ate a balanced diet full of omega-3 fats, antioxidants and low glycemic carbohydrates like whole grains.
- To manage stress, participants performed daily relaxation exercises. Small notes that stress causes the body to release cortisol, a hormone that can impair memory and damage brain memory cells.
Brain function was tested before and after the 14-day study, using positron emission tomography (PET) scans to measure brain activity. Participants who followed the healthy longevity lifestyle plan demonstrated a five percent decrease in brain metabolism in the part of the brain directly linked to working memory called the dorsal lateral prefrontal cortex.
"The finding suggests that for participants who had followed the healthy longevity program, the brain functioned more efficiently and didn't need to use as much glucose to perform effectively," Small said.
In addition, compared to the control group, participants also performed better in verbal fluency, a cognitive function controlled by the same brain region.
"The research demonstrates that in just 14 days, simple lifestyle changes can not only help overall health, but also improve memory and brain function," Small said.
-American Journal of Geriatric Psychiatry
January 10, 2006
Zeroing in on a gene: Region of DNA strongly associated with Alzheimer’s disease -An international team of researchers, led by investigators at the School of Medicine, are zeroing in on a gene that increases risk for Alzheimer's disease. They have identified a region of chromosome 10 that appears to be involved in risk for the disease that currently affects an estimated 4.5 million Americans.
Alzheimer's Vaccine that Restores Memory in Mice Revealed by Researchers shows promise of reversing memory loss, slowing effects of Alzheimer's
New study finds that older Americans may improve memory by exercising their brains and bodies - Research presented at ACNP Annual Meeting
New research released today at the American College of Neuropsychopharmacology's Annual Meeting found that older Americans may improve their memory by making simple lifestyle changes - including memory exercises, physical fitness, healthy eating and stress reduction. The study was conducted at the University of California, Los Angeles (UCLA) and funded by the Fran and Ray Stark Foundation Fund for Alzheimer's Disease Research, the Judith Olenick Elgart Fund for Research on Brain Aging, and the Parlow-Solomon Professorship on Aging.
"We've known for years that diet and exercise can help people maintain their physical health, which is a key component of healthy aging," says lead investigator, Gary Small, M.D., Professor of Psychiatry and Behavioral Sciences at the David Geffen School of Medicine at UCLA, " But maintaining mental health is just as important. Now we have evidence which suggests that people can preserve their memory by adding memory exercises and stress reduction to this routine."
The study was the first to test the impact of combining memory exercises and stress reduction with a healthy diet and exercise to improve memory. In the 14-day study, subjects with normal baseline memory performance scores were randomly assigned to two groups (sample size of 17 individuals). In the test group, subjects following a memory improvement plan which included:
- Memory Training - Brainteasers, crossword puzzles and memory exercises, which emphasized verbal skills, were conducted throughout the day to stimulate the brain.
- Healthy Diet - Participants ate five meals daily, which included a balanced diet rich in omega-3 fats, low-glycemic index carbohydrates (e.g., whole grains) and antioxidants. Eating five small meals throughout the day prevents dips in blood glucose levels and glucose is the primary energy source for the brain.
- Physical Fitness - Brisk daily walks and stretching were done daily to promote physical fitness, which has been found to reduce the risk of Alzheimer's Disease.
- Stress Reduction - Participants used stretching and relaxation exercises to manage stress. Stress causes the body to release cortisol, which plays an important role in memory preservation. Cortisol can impair memory and has been found to shrink the memory centers in the brain.
In the control group, subjects did not make any behavior modifications.
Immediately before and after the 14-day study, each participant's brain function was tested using positron emission tomorgraphy (PET) scans to measure activity throughout the brain. After the 14-day study, participants following the memory improvement plan recorded a 5% decrease in brain metabolism in the dorsal lateral prefrontal region of the brain, which is directly linked to working memory and other cognitive functions, suggesting that they were using their brain more efficiently. Furthermore, these subjects reported improved memory, and demonstrated better performance on a cognitive measure controlled by this same brain region.
"Most people do not realize that they are in control of their memory as they get older," declared Dr. Small, "But this research demonstrates that it is possible, in just 14 days, to make simple lifestyle changes that will not only improve memory and brain function, but also will improve overall health and wellness."
The next step in this research is to better understand the specific effect of each individual component of the memory improvement plan to determine which combination of healthy lifestyle strategies produces optimal results.
Thursday, March 10, 2005
CHICAGO, Mar 10, 2005 (United Press International via COMTEX) -- Chicago scientists using mice to study Alzheimer's disease say a use-it-or-lose-it approach may be a key to keeping one's mind in good working order.
The University of Chicago team, in an article set for publication Friday in the journal Cell, found that mice who kept their brains and bodies busy in an "enriched" environment of chew toys, running wheels, and tunnels had lower levels of the peptides and brain plaques associated with Alzheimer's disease compared to mice raised in more sparse conditions.
Levels of b-amyloid peptides, which clump together to form the brain "tangles" or plaques that are toxic to nerve cells in Alzheimer's disease, were significantly lower in the enriched mice.
The enriched mice may have been better equipped than their less-stimulated counterparts to sweep these peptides out of the brain, according to the researchers' analysis of gene and enzyme expression in the animals.
"This goes back to the old idea of use it or lose it, that using your brain keeps it more active," one of the researchers said. "It's more common sense than anything, but what we didn't previously appreciate is that it might affect the pathology that is characteristic of Alzheimer's disease."
Monday, March 7, 2005
PROVIDENCE, R.I., Mar 07, 2005 (United Press International via COMTEX) -- Rhode Island researchers have discovered insulin and its related proteins are produced in the brain and both are linked to Alzheimer's disease.
"What we found is that insulin is not just produced in the pancreas, but also in the brain and we discovered that insulin and its growth factors, which are necessary for the survival of brain cells, contribute to the progression of Alzheimer's," said senior author Suzanne de la Monte, a neuropathologist at Rhode Island Hospital and a professor at Brown Medical School. "This raises the possibility of a Type 3 diabetes."
Now that scientists have pinpointed insulin and its growth factors as contributors to Alzheimer's, it opens the way for targeted treatment to the brain and changes the way Alzheimer's disease is viewed, according to de la Monte.
The findings are reported in the Journal of Alzheimer's Disease.
Thursday, March 3, 2005
AMSTERDAM (Reuters) - Regular exercise and a healthy diet could go a long way to reducing the risk of developing Alzheimer's disease, a neurologist said on Thursday.
A recent Finnish study showed that middle-age people taking regular exercise at least twice a week could reduce their risk of developing Alzheimer's disease by 50 percent in old age, Dr. Miia Kivipelto said at a conference in Amsterdam.
"An active lifestyle, both physical, mental and social, is preventive. It's never too early to start to prevent Alzheimer's disease," said Kivipelto, who is an Alzheimer's disease specialist at Stockholm's Gerontology Research Center.
An estimated 12 million people worldwide have from Alzheimer's disease, the leading cause of dementia in the elderly. There is no cure for this condition that robs people of their memory and mental ability, but drugs have been approved to alleviate symptoms.
Studies have shown that people with high blood pressure, high cholesterol and obesity could have a greater risk of Alzheimer's disease or other dementia than those with a more active, healthy lifestyle, she said.
People could reduce their risk by getting regular check-ups to monitor blood pressure, cholesterol and weight, she said at a conference on old age organized by Britain's Royal College of Psychiatrists. Other recent studies show that elderly people who take regular walks are less likely to have dementia. Mental activities such as reading and doing crossword puzzles also help to slow mental decline.
Wednesday, March 2, 2005
IRVINE, Calif., Mar 02, 2005 (United Press International via COMTEX) -- A protein that builds up on neurons in the brain marks the onset of memory decline associated with Alzheimer's disease, researchers said Wednesday.
Accumulation of the protein, beta amyloid, is the trigger that fires the loss of memory in the degenerative disorder that currently affects as many as 5 million American adults, concludes a study by the University of California Irvine.
Alzheimer's sufferers are unable to clear the excess protein buildup that healthy brains can remove.
Researcher said the discovery underscores the need to develop methods to keep the memory-robbing beta amyloids from building up in one's brain.
Without effective therapies, researchers said it is estimated the number of Americans suffering from Alzheimer's will jump to 13 million by 2050.
The research is reported in the journal Neuron.
Thursday, February 24, 2005
Blockages in cellular pathways called axons appear to occur much earlier in those with Alzheimer's disease than once thought, researchers report in a new study.
Axons connect brain cells to each other and carry electrical signals and chemical supplies throughout the brain. Thought, perception, memory and learning can occur when nerve impulses are carried along axons.
The pathways also extend to muscles and organs.
Alzheimer's is a degenerative condition that strikes the parts of the brain guiding memory and language, and generally becomes more common in people over age 60. However, it is not the result of normal aging. An estimated 4 million Americans suffer from the disease, for which there is no known cure.
Researchers at the University of California-San Diego studied both mouse models of Alzheimer's and brain tissue from human Alzheimer's patients who died when their disease was in its early stages.
They report Friday in the journal Science that they found abnormal amounts of proteins, cell parts and small cysts clogging the axons - like a rock in a garden hose - in both the mice and in the human brain tissue of early Alzheimer's patients more than a year before other symptoms were evident.
While scientists had known that transport within axons was blocked in late-stage Alzheimer's, the study is the first to show that the process begins early. This could help both in diagnosis and finding treatment for the disease.
It also marks the first evidence of a link between the two abnormalities that are the disease's hallmark twisted, insoluble brain fibers called neurofibrillary tangles and amyloid plaques, excessive amounts of protein fragments that the body naturally produces.
Thursday, February 17, 2005
NEW YORK (Reuters Health) - Mental tasks take an extra effort for healthy non-demented older adults with a genetic variation called APOE-e4, which has been linked to an increased risk of developing Alzheimer's disease, research shows.
On tests of learning and memory, brain scans show that people with APOE-e4 apparently have to work harder to achieve scores comparable to those reached by people with the APOE-e3 variant.
"This study confirms alterations in brain activity during learning in healthy older people at genetic risk for Alzheimer's disease," Dr. Mark W. Bondi from the VA San Diego Healthcare System told Reuters Health.
Bondi and his colleagues had 20 non-demented adults (average age, 76) with normal learning and memory capabilities complete a picture-encoding task while undergoing magnetic resonance imaging.
In multiple brain regions, the 10 people with the APOE-e4 gene displayed greater intensity and extent of brain activation while learning new pictures, compared with the 10 individuals with the APOE-e3 allele.
The APOE-e4 group also displayed lower brain responses in another area during tasks of learning and memory, the researchers report in the journal Neurology.
"The implications of this finding," Bondi told Reuters Health, "include the possibility of providing new methods for identifying the earliest stages of Alzheimer's disease."
Tests based these findings may "help us recognize brain changes early so that we can identify the people at highest risk for the disease, with the goal of providing them with treatment more quickly and efficiently," he added.
SOURCE: Neurology, February 8, 2005.
Friday, January 14, 2005
Anti-Cholesterol Drug May Block Amyloid Pathology in Alzheimer’s Disease
A drug designed to inhibit cholesterol production may also block the production of amyloid, a hallmark of Alzheimer’s disease (AD). In a mouse model of the disease the drug CP-113,818 reduced amyloid buildup by up to 99 percent and worked for up to 2 months without any evidence of toxicity. The study was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS).
CP-113,818 was previously shown to reduce amyloid in nerve and other cells. The drug inhibits the cholesterol-modifying enzyme ACAT (acyl-coenzyme A:cholesterol acyltransferase) that allows the buildup of amyloid. In the current study, investigator Dora M. Kovacs, Ph.D., director of the Neurobiology of Disease Laboratory at Massachusetts General Hospital and colleagues in the U.S. and Austria tested the hypothesis that ACAT inhibition would also inhibit the amyloid-beta peptide involved in AD.
The researchers first tested the drug on 18 non-transgenic mice over 21 days using different dose levels of slow-release pellets that were surgically inserted under the skin. The investigators studied dose levels ranging from 0.2 to 7.1 mg/kg per day. At the highest daily dose given, CP-113,818 reduced total cholesterol levels by 29 percent without any apparent effect on food consumption or body weight. Hepatic free cholesterol and cholesteryl-esters also decreased dramatically at lower doses, in a dose-dependent manner.
Slow-release pellets containing a 60-day supply of the highest dose of the drug per day were then surgically inserted under the skin of 12 mice specially bred to carry various forms of familial AD. Twelve control mice received a placebo pellet. The study was halted just before 2 months to ensure continued release of the drug. The scientists found no evidence of toxicity in mice receiving the drug and blood cholesterol levels were reduced to levels similar to normal mice.
Amyloid plaque was reduced by 88 percent in brain tissue in mice who received CP-113,818 and up to 99 percent in the hippocampus of the female transgenic mice. These findings, together with chemical analyses conducted on the mouse brains, suggest that the ACAT inhibitor prevents accumulation of newly formed plaques and is highly effective in reducing the amount of plaque already there. The treated mice also performed better in a test of cognitive function.
Although CP-113,818 is not optimal for clinical testing in humans, a similar ACAT-inhibiting drug, CI-1011, is currently in phase III trials for vascular disease and atherosclerosis. Researchers have previously shown that statin drugs (or statin-like compounds) can dramatically reduce amyloid pathology in different animal models when administered before amyloid begins to accumulate.
“Our findings suggest that slow-release administration of ACAT inhibitors may be a novel strategy to treat and prevent AD, either alone or in combination with statins,” said Dr. Kovacs. Diane Murphy, Ph.D., an NINDS program director for neurodegenerative disorders, said "Although much more work is needed before these inhibitors can be tested in humans, this study is a promising and exciting first step in determining if ACAT inhibitors could be given to patients to reduce amyloid in Alzheimer’s disease.”
Brain Produces New Cells in Multiple Sclerosis
The brain produces new cells to repair the damage from multiple sclerosis (MS) for years after symptoms of the disorder appear, according to a recent study. However, in most cases the cells are unable to complete the repairs. These findings suggest that an unknown factor limits the repair process and may lead to new ways of treating this disorder."The brain is making a serious attempt to repair the damage," says Bruce D. Trapp, Ph.D., of the Cleveland Clinic Foundation in Ohio, who led the study. The findings are consistent with those of other recent studies showing that the adult brain has the capacity to replace cells, he adds. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS) and appears in the January 17, 2002, issue of The New England Journal of Medicine.
In patients with multiple sclerosis, brain inflammation in random patches, or lesions, leads to destruction of myelin, the fatty covering that insulates nerve cell fibers called axons in the brain and spinal cord and aids in transmission of signals to other neurons. This inflammation causes the myelin to deteriorate and leads to the symptoms of MS. Previous studies have shown that some brain lesions are repaired during the early years of multiple sclerosis. However, many other lesions are not repaired.
In the study, Dr. Trapp and colleagues examined brain tissue obtained during autopsies of 10 patients with MS to see if new myelin-producing cells, called oligodendrocytes, were being produced in the chronic MS lesions. They found that most of the lesions contained newly produced oligodendrocytes. The percentage of lesions from each brain that had these new cells decreased as the duration of the disease increased, but the decline was not related to the type of MS the patients had or to their ages at death. The new oligodendrocytes extended "arms" that produced myelin-related proteins and grew around the damaged axons as if they were trying to repair the myelin. However, in most cases the axons were not repaired.
One of the central questions in MS research is how to promote myelin repair. Many researchers have concentrated on increasing the number of oligodendrocytes through stem cell transplantation or other means. However, this study suggests that problems with the axons or with the tissue that surrounds them may prevent remyelination. Many of the axons that were not remyelinated looked abnormal, whereas remyelinated axons appeared healthy. This suggests that therapies which prevent axon degeneration or help oligodendrocytes complete the repair process in other ways may be necessary. More research is needed to identify drugs that may be useful for this purpose, says Dr. Trapp. While the study shows that the brain's attempts to repair itself decrease over time, new cells were produced even in patients who had had MS for as long as 15 years, implying that there is a long window of opportunity for treatment.
Researchers must now determine how long the new oligodendrocytes survive in the brain and whether the brain can produce enough of them to repair all the damage from MS, says Dr. Trapp. If the brain produces enough new cells on its own, then transplantation of additional cells may not be necessary. Research using brain scanning or other techniques may help to identify patients who are most likely to benefit from these therapies.