The brain is like any other muscle in the body that gets stronger with proper exercise and shrivels if neglected. To keep the brain functioning at its full potential, researchers say there are specific lifestyle adjustments which can be made that can benefit many important brain functions.
Memory, one of the pivotal functions the brain performs, can be enhanced by staying mentally active, eating right, and participating in some form of physical exercise on a daily basis.
Mental exercise
Working out the mind with strategies to increase memory capacity are not just for the aging, but can also be used by the younger generations for some short-term payoffs, UCLA memory researchers said.
Recent studies have found that after normal adults are thought to use these strategies for remembering, their brain activity has become more efficient according to scans, said Gary Small, professor of clinical psychiatry at UCLA.
These mental exercises can be easily remembered as the “look, snap and connect,” Small said.
The first step in remembering is to look and focus your attention on your subject, he added.
“You should never multitask since it hurts your ability to attend to information and will cause you not to remember,” Small said.
The next step, snap, involves creating a visual image of the subject matter that you are trying to remember, he added. This helps to recall and retrieve the information later.
Medical school students often use these sorts of techniques when required to memorize complex anatomy, said Linda Ercoli, director of geriatrics psychology at the UCLA Semel Institute.
“The idea is to associate them with things that you already know that have meaning for you,” Ercoli said. “This will allow the processing to happen on a more meaningful level.”
The final step is to connect, which consists of putting the newly learned information into context, Small said.
“If you just memorize facts, it will be in and out,” Small said. “You need to rehearse and repeat the information; a good way to do this in class is to take good notes in class and write summaries after.”
If strategies like this are applied to everyday life, people can bring their memory abilities up to their full potential and even prevent future degenerative conditions of the brain, Small added.
Diet
The brain is affected by everything you put into your body, including your diet.
Recent studies have found that a well-balanced diet can help ward off the appearance of all kinds of mental disorders, including those that involve memory loss like Alzheimer’s.
Fernando Gomez-Pinilla, professor of neurosurgery at UCLA, analyzed 160 studies to understand how food can impact the brain.
“The basic idea of the research is that the capacity of the brain depends on the type of life we have,” Gomez-Pinilla said. “Essentially, the simple things we do may have an important influence on the brain.”
It was discovered that omega-3 fatty acids, found in salmon, kiwi, and walnuts can improve memory abilities and prevent mental disorders as well.
Gomez-Pinilla focused also on the synapses in the brain, which connect brain cells, where it is believed learning and memory occur.
Another study found that children exposed to a diet rich with this brain vitamin, omega-3, performed better in school and had fewer behavioral problems.
Other brain enriching foods include spinach, rich with folic acid which is essential for brain function, Gomez-Pinilla said.
There are foods to stay away from that can cause damage to many systems in the brain, including memory, Gomez-Pinilla said.
Junk foods that are high in saturated fats have been shown to negatively impact the synapses of the brain, he added. Certain fruits, like blueberries, have the opposite effect since they are rich antioxidants and prevent oxidative damages which accumulate in the brain.
Healthy diets are essential not only for physical well-being, but also for the mind, Gomez-Pinilla said.
Exercise and stress
Getting your blood pumping through exercise has been linked to increased brain function and memory.
Several studies using animal models have found exercise can help increase cognitive function in animals as well as reduce the mental decay which occurs with aging, said Fernando Gomez-Pinilla, professor of neurosurgery at UCLA.
“Doing 30 minutes of running exercise a day can make a big short-term difference in memory and mental function,” Gomez-Pinilla said.
The best type of exercise is cardiovascular since it is good for the heart, hence good for the brain, said Gary Small, professor of clinical psychiatry at UCLA.
This form of exercise, like running, gets more blood flowing to the brain, he added.
However, there may be other reasons why exercise has been shown to work wonders for getting the brain in shape.
The endorphin rush which hits the body during exercise may also be a brain-strengthening mechanism.
Other findings suggest that high amounts of stress, which release the stress hormone, cortisol, in to the body can interfere with memory production and storage, Small said.
In terms of test taking and study habits, Small said that cramming is one of the worst methods, especially due to the elevated levels of stress in addition to lack of sleep.
Small added that many students can get by fine cramming, partying on the weekends, and getting little or no sleep because the teenage years up to the early 20s are the prime time for learning and brain power.
But, cramming may work now, but it won’t a few years down the line, Small said.
So the time is now to start taking care of your memory, Small added.
Source: University of California, Los Angeles (http://www.dailybruin.ucla.edu/news/2008/sep/08/choose-healthy-lifestyle-keep-your-brain-peak-shap/)
The most comprehensive-to-date genomic analysis of a cancer – the deadly brain tumor glioblastoma multiforme – shows previously unrecognized changes in genes and provides an overall view of the missteps in the pathways that govern the growth and behavior of cells, said members of The Cancer Genome Atlas Research Network in a report that appears online today in the journal Nature.
“This was a big thrust for the public project,” said Dr. Richard Gibbs, director of the Baylor College of Medicine Human Genome Sequencing Center, a member of the network and a co-author of the paper. “This answers the big question about whether the cancer genome project is worthwhile. The results show that it is—definitely.” The BCM center, the Genome Sequencing Center at Washington University School of Medicine in St. Louis, Mo., and the Broad Institute of MIT and Harvard in Cambridge, Mass., led the effort that included many members from across the nation.
This interim analysis of 91 tumors and 623 genes provides important clues about how the disease originates and progresses in cells and how it eludes the effects of potent anti-cancer drugs and radiation, said Dr. David Wheeler, associate professor in the Genome Sequencing Center and a co-author of the report. It could provide researchers with clues about how to treat the disease. The Baylor Human Genome Sequencing Center was a major component in the effort to sequence the genes and identify mutations and changes that affected the ways cells react.
“Studies like this show the breadth of mutation across many genes,” said Wheeler. “We can see the mutations in all the genes of each pathway that control growth, replication and death in the cancer cell. Researchers have never seen the whole landscape like this before, and it’s providing many new insights into strategies to diagnose and treat cancer.”
The ultimate goal of the project is to sequence the entire exome – that portion of the genetic blueprint that provides the code for proteins – of the tumor, said Wheeler. In fact, he said, the goal is to sequence genes in 500 brain cancer samples, but the network decided to publish preliminary results.
“When we pulled everything together with just 91 samples, the results were so interesting and important for treatment that we felt we should publish before the end of the project,” he said.
Glioblastoma is the most common primary brain tumor. Most people live approximately one year after diagnosis. Understanding this cancer could result in better forms of treatment.
The analysis identified some genes known to cause cancer but whose role in glioblastoma had been previously underestimated, he said. For example, the genes ERBB2 (known to be implicated in breast and other cancers) and NF1 (neurofibromatosis gene 1 involved in a variety of tumors) were both found to be frequently mutated in this brain tumor. Other genes that previously had no known role in glioblastoma such as PIK3R1, a gene involved in regulating the metabolic actions of insulin were also found mutated in a variety of tumors.
In addition, the analysis gave scientists a wide view of how cell pathways are altered during the initiation and growth of glioblastoma.
“If we know what pathways are key to the formation of a tumor, we can design drugs to block those pathways,” said Wheeler. “In cancer, key pathways are co-opted to make the cell grow and divide in an uncontrolled fashion.”
For example, the TP53 pathway tells mutated cells to die in a process called apoptosis.
“It’s a fail-safe mechanism,” said Wheeler. “If a cell starts to become cancerous, p53 causes the cell to kill itself. If that pathway is knocked out, the cell avoids the fail-safe mechanism and can continue to divide.”
Other pathways involved in the sequencing effort are also disrupted to allow the cancer to grow, he said.
Funding for this work came from the National Institutes of Health.
Others who took part in the sequencing effort at BCM include Donna Muzny, Margaret Morgan, Steve Scherer, Aniko Sabo, Lynn Nazareth, Lora Lewis, Otis Hall, Yiming Zhu, Yanru Ren, Omar Alvi, Jiqiang Yao, Alicia Hawes, Shalini Jhangiani, Gerald Fowler, Anthony San Lucas, Christie Kovar, Andrew Cree, Huyen Dinh, Jireh Santibanez, Vandita Joshi, Manuel L. Gonzalez-Garay, Christopher A. Miller, Aleksandar Milosavljevic and Larry Donehower.
Other institutions involved in this work include the Dana-Farber Cancer Institute in Boston; Harvard Medical School and The Brigham and Women’s Hospital in Boston; Memorial Sloan-Kettering Cancer Center in New York; The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins in Baltimore; the National Cancer Institute Center for Bioinformatics in Bethesda, Md; the University of North Carolina Lineberger Comprehensive Cancer Center in Chapel Hill; SRA International Inc., in Fairfax, Va.; HudsonAlpha Institute for Biotechnology in Huntsville, Ala.; Lawrence Berkeley National Laboratory in Berkeley, Calif., and the International Genomics Consortium in Phoenix, Ariz.
Source: Baylor College of Medicine (http://www.bcm.edu/news/item.cfm?newsID=1200)
MIT engineers report a new approach to identifying protein structures key to Alzheimer’s disease, an important step toward the development of new drugs that could prevent such structures from forming.
In the Aug. 22 issue of PLoS (Public Library of Science) Computational Biology, the researchers describe one such structure uncovered using a new computer-based technique.
Collin M. Stultz, the leader of the work and the W.M. Keck Associate Professor of Biomedical Engineering in the Department of Electrical Engineering and Computer Science, noted that the same general approach could also be applied to certain proteins associated with cancer.
Alzheimer’s disease is the most common form of dementia, affecting some five million Americans, according to the Alzheimer’s Association. And due to the growing elderly population, that number “is expected to reach a staggering 13.2 million by 2050,” said Stultz, who is also affiliated with the Harvard-MIT Division of Health Sciences and Technology (HST) and MIT’s Research Laboratory of Electronics.
Existing therapies, he continued, “do not adequately slow the rate of neurodegeneration in Alzheimer’s patients. As such, there is an urgent need to develop new treatments for Alzheimer’s dementia.”
Stultz’s approach to the problem combines his background in engineering and medicine (he holds a PhD and MD, and is a practicing cardiologist with appointments at Brigham and Women’s Hospital and the West Roxbury Veterans Administration Hospital). In his work, biochemical experiments inform a novel computer modeling technique aimed at better understanding one type of protein associated with the disease.
Alzheimer’s is characterized by two kinds of proteins — amyloid and tau — that aggregate in the brain. Stultz and co-author Austin Huang, an HST graduate student, have focused on determining the structure of tau.
But there’s a problem. “Tau is ‘natively unfolded,’ or floppy, so in solution it moves around a lot and can adopt many different structures,” Stultz said, much like the individual strands in a bowl of cooked spaghetti. Contrast that to the vast majority of other proteins, whose individual strands have similar structures, like the individual strands of uncooked spaghetti.
“With a ‘normal’ protein,” Stultz said, “you can measure the lengths of individual molecules and the average will be a pretty good description of any one.” Tau molecules, however, “are all over the place — they’re so diverse that it’s difficult to get one measurement that describes all of the possible structures.”
That complicates the hunt for specific tau structures associated with Alzheimer’s (not all tau is bad).
Stultz and Huang approached the problem as engineers, breaking it down into steps. Using a method they developed called Energy-minima Mapping and Weighting (EMW), they asked a computer to come up with all possible structures of tau that are consistent with an average set of experimental data.
“We generated lots and lots of structures for both normal tau and a mutant form” associated with an increased risk for Alzheimer’s, Stultz said. By comparing the two sets, the researchers found one structure that was more common in the mutant form — and therefore likely to “play a role in the pathologic process.” That structure, in turn, could then become the target for a new drug.
Stultz notes that the current work focused on one tau mutant associated with Alzheimer’s, but there are several others. So eventually he hopes to use EMW to create “a list of all types of suspect conformations for known tau mutants. Then, from that list, we can design drugs for each.”
This work was sponsored by a Jonathan Allen Junior Faculty Award.
Source: MIT News, Elizabeth A. Thomson (”http://web.mit.edu/newsoffice/2008/alzheimers-protein-0821.html“)
Researchers at Johns Hopkins are reporting what is believed to be the most conclusive evidence to date that inadequate levels of vitamin D, obtained from milk, fortified cereals and exposure to sunlight, lead to substantially increased risk of death.
In a study appearing in the Archives of Internal Medicine online Aug. 11, the Johns Hopkins team analyzed a diverse sample of 13,000 initially healthy men and women participating in an ongoing national health survey and compared the risk of death between those with the lowest blood levels of vitamin D to those with higher amounts. An unhealthy deficiency, experts say, is considered blood levels of 17.8 nanograms per milliliter or lower.
Of the 1,800 study participants known to have died by Dec. 31, 2000, nearly 700 died from some form of heart disease, with 400 of these being deficient in vitamin D. This translates overall to an estimated 26 percent increased risk of any death, though the number of deaths from heart disease alone was not large enough to meet scientific criteria to resolve that it was due to low vitamin D levels.
Yet researchers say the finding does highlight a trend, with other studies linking shortages of vitamin D to increased rates of breast cancer and depression in the elderly. And earlier published findings by the team, from the same national study, have established a possible tie-in, showing an 80 percent increased risk of peripheral artery disease from vitamin D deficits.
Researchers note that other studies in the last year or so in animals and humans have identified a connection between low levels of vitamin D and heart disease. But these studies, they say, were weakened by small sample numbers, lack of diversity in the population studied and other factors that limited scientists’ ability to generalize the findings to the public at large.
“Our results make it much more clear that all men and women concerned about their overall health should more closely monitor their blood levels of vitamin D, and make sure they have enough,” said study co-lead investigator Erin Michos.
“We think we have additional evidence to consider adding vitamin D deficiency as a distinct and separate risk factor for death from cardiovascular disease, putting it alongside much better known and understood risk factors such as age, gender, family history, smoking, high blood cholesterol levels, high blood pressure, lack of exercise, obesity and diabetes,” she said.
Vitamin D is well-known to play an essential role in cell growth, in boosting the body’s immune system and in strengthening bones.
“Now that we know vitamin D deficiency is a risk factor, we can better assess how aggressively to treat people at risk of heart disease or those who are already ill and undergoing treatment,” said Michos, who added that test screening for nutrient levels is relatively simple. It can, she said, be made part of routine blood work and be done while monitoring other known risk factors, including blood pressure, glucose and lipid levels.
Heart disease remains the nation’s leading cause of death, killing more than a million Americans each year. Nearly 10 percent of those with the condition have not one identifiable, traditional risk factor, which the experts say is why a considerable extent of the disease goes unexplained.
Michos, an assistant professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute, recommends that people boost their vitamin D levels by eating diets rich in such fish as sardines and mackerel, consuming fortified dairy products, taking cod-liver oil and vitamin supplements and in warmer weather briefly exposing skin to the sun’s vitamin D — producing ultraviolet light.
Aware of the cancer risks linked to too much time spent in the sun, Michos says that as little as 10 to 15 minutes of daily exposure to the sun can produce sufficient amounts of vitamin D to sustain health. The hormonelike nutrient controls blood levels of calcium and phosphorus, essential chemicals in the body.
Michos says that if vitamin supplements are used, there is no evidence that more than 2,000 international units per day do any good. Study results show that heart disease death rates flattened out in participants with the highest vitamin D levels (above 50 nanograms per milliliter of blood), signaling a possible loss of the vitamin’s protective effects at too-high doses.
The U.S. Institute of Medicine suggests that an adequate daily intake of vitamin D is between 200 and 400 international units (or blood levels nearing 30 nanograms per milliliter). Previous results from the same nationwide survey showed that 41 percent of men and 53 percent of women are technically deficient in the nutrient, with vitamin D levels below 28 nanograms per milliliter.
Michal Melamed, study co-lead investigator, who started the research as a clinical fellow at Johns Hopkins, says that no one knows yet why or how vitamin D’s hormonelike properties may protect the heart, but she adds that there are plenty of leads in the better known links the vitamin has to problems with muscle overgrowth and high blood pressure, in addition to its control of inflammation, which scientists are showing plays a stronger role in all kinds of heart disease. But more research is needed to determine the nutrient’s precise biological action.
Researchers say their next steps are to test various high doses of vitamin D to find out if the nutritional supplementation results in fewer deaths and lower incidence of heart disease, including heart attack or moments of prolonged and severe chest pain.
The team also plans to investigate what biological triggers, such as obesity or hypertension, might offset or worsen the action of vitamin D on heart muscle, or whether vitamin D sets off some other reaction in the heart.
Melamed says that because vitamin D levels are known to fluctuate in direct proportion with daily physical activity, the growing epidemic of obesity and indoor sedentary lifestyles lend more urgency to act on the vitamin D factor.
Funding for this study was provided by the National Institutes of Health, P.J. Schafer Cardiovascular Research Fund and Paul Beeson Physician Faculty Scholars in Aging Program. Michos has received previous consulting fees from vitamin D therapeutics manufacturer Abbott Pharmaceuticals. The terms of these arrangements are being managed by The Johns Hopkins University in accordance with its conflict of interest policies.
Other Johns Hopkins researchers involved in this study, conducted solely at Johns Hopkins, were Wendy Post and Brad Astor. Melamed is now an assistant professor at the Albert Einstein College of Medicine of Yeshiva University.
Source: John Hopkins Medicine, David March (http://www.jhu.edu/~gazette/2008/18aug08/18vitamind.html)