How Your Inner Athlete Makes You Smarter

Athletes and people who exercise not only have better bods — they have better brains too, a host of studies have now firmly established. ... Continue Reading

Alzheimer's could be caused by glucose inefficiencies

Sufferers of Alzheimer's disease who also have a mother with the illness may have the disease because of an inability of the brain to efficiently use glucose, according to new findings. ... Continue Reading

Injection Of Human Umbilical Cord Blood Helps The Aging Brain, Study Shows

When human umbilical cord blood cells (UCBC) were injected into aged laboratory animals, researchers at the University of South Florida (USF) found improvements in the microenvironment of the hippocampus region of the animals’ brains and a subsequent rejuvenation of neural stem/progenitor cells.

The research presented the possibility of a cell therapy aimed at rejuvenating the aged brain.

“Brain cell neurogenesis decreases dramatically with increasing age, mostly because of a growing impoverishment in the brain’s microenvironment,” said co-author Alison Willing, PhD, of the USF Center of Excellence for Aging and Brain Repair. “The increase in neurogenesis we saw after injecting UCBCs seemed to be due to a decrease in inflammation.”

According to lead author Carmelina Gemma, Ph.D., of the James A. Haley Veterans Administration Medical Center (VA) and USF, the decrease in neurogenesis that accompanies aging is a result of the decrease in proliferation of stem cells, not the loss of cells.

“In the brain, there are two stem cell pools, one of which resides in the hippocampus,” explained graduate student and first author Adam Bachstetter. “As in other stem cell pools, the stem cells in the brain lose their capacity to generate new cells. A potent stressor of stem cell proliferation is inflammation.”

Prior to this study, the research team led by Paula C. Bickford, Ph.D., of the VA and USF found that reducing neuroinflammation in aged rats by blocking the synthesis of the pro-inflammatory cytokine IL1 rescued some of the age-related decrease in neurogenesis and improved cognitive function.

“We think that UCBCs may have a similar potential to reduce inflammation and to restore some of the lost capacity of stem/progenitor cells to proliferate and differentiate into neurons,” said Dr. Bickford.

The study found that the number of proliferative cells increased within 24 hours following the UCBC injections into the aged laboratory rats and that the increased cell proliferation continued for at least 15 days following a single treatment.

“We have shown that injections of UCBCs can reduce neuroinflammation,” concluded co-author Paul R. Sanberg, Ph.D. D.Sc. director of the Center of Excellence for Aging and Brain Repair. “Our results raise the possibility that a cell therapy could be an effective approach to improving the microenvironment of the aged brain and restoring some lost capacity.”

Citation: Bachstetter, AD, Pabon, MM, Cole, MJ, Hudson, CE, Sanberg, PR, Willing, AE, Bickford, PC, Gemma, C. Peripheral injection of human umbilical cord blood stimulates neurogenesis in the aged rat brain. BMC Neuroscience, 9(1), 2008, 22 (Epub ahead of print).

The USF study was supported by the National Institutes of Health and the VA Medical Research Service.

'Testosterone link' to depression

Older men with lower levels of the male sex hormone testosterone in their blood may be more prone to depression, a study suggests.
A study of about 4,000 men aged over 70 found those with lowest testosterone were three times more likely to be depressed than those with the most.

Researchers suspect the hormone may affect levels of key brain chemicals.

The study, by the University of Western Australia, features in Archives of General Psychiatry.

Research has found that women are more likely to be depressed than men until the age of 65, when the difference between the genders almost disappears.

Testosterone levels decline with age - but there is wide variation.

The Australian team studied 3,987 men over the age of 70. Each gave blood samples and took part in tests to determine whether they were depressed.

In total 203 of the participants were assessed as being depressed.

They had significantly lower levels of both total testosterone, and free testosterone, which is not bound to proteins.

The researchers then adjusted the data to take account of factors such as educational attainment and body fat levels.

They found those men whose level of free testosterone was in the bottom 20% were three times more likely to be depressed than those in the top 20%.

The researchers said further work was required to confirm their findings.

But their work raised the possibility that treatment to boost testosterone levels in older men may be an effective way to treat depression.

Raised death risk

A previous study of 800 men over the age of 50 found that those with low levels of testosterone had a 33% increased risk of death over an 18-year period than those with higher levels.

They appeared significantly more likely to have a cluster of risk factors associated with cardiovascular disease and diabetes.

This raises the possibility that men with low testosterone levels may be prone to depression because they are also more likely to be in poor physical health.

However, the Australian researchers concluded that this could not fully explain the link, and that some other factor must also be in play.

Testosterone replacement therapy has also been shown to help elderly men with mild Alzheimer's disease.

Research has suggested that levels of testosterone in men of all ages are falling.

Professor David Kendall, an expert in pharmacology at the University of Nottingham, said there was a wealth of evidence to show that testosterone levels were linked to mood.

For instance, farmers had long castrated their stock to pacify them.

Research on animals had also shown that removal of their gonads blocked the action of anti-depressants on key mood-controlling chemicals in the brain.

"It would be no surprise that low testosterone reduces mood," he said.

"Testosterone therapy offers a relatively simple intervention, potentially, for some groups of older depressives with hypogonadism (low production of sex hormones)."

Professor Stafford Lightman, a hormone expert at the University of Bristol, said testosterone potentially had many small effects which could raise the risk of depression. For instance, low levels had been linked to poor cognitive performance.

However, he warned that depression, particularly in elderly people, was often the result of many different, inter-relating factors, and warned against placing too much emphasis on one in isolation.

"My view is that low testosterone could be a contributory factor to depression, but probably not a very powerful one," he said.

http://news.bbc.co.uk/1/hi/health/7274481.stm

How to Age-Proof Your Memory

Drink a cocktail, gossip, and other surprising ways to boost your brain power
by Ross Weale

Health magazine contributor Roshini Raj, MD, gives tips to boost your memory on Today, March 3, 2008.



DR. ROSHINI RAJ
Roshini Raj, MD, a Health magazine contributor and part of the magazine's Health Expert Network, is board-certified in gastroenterology and internal medicine with degrees from the New York University School of Medicine and Harvard University. Currently Dr. Raj is an attending physician at NYU Medical Center's Tisch Hospital in New York City. She also serves as an assistant professor at the NYU School of Medicine, and she has a special interest in women's health and cancer screening. She has also published several research articles on colon-cancer screening.

Dr. Raj has discussed health topics on numerous television outlets, including NBC's Today show, ABC's Good Morning America, CNN, FOX News, and Discovery Health. She has been quoted in publications such as the New York Times, the Wall Street Journal, Men's Health, Women's Health, and Fitness on the state of health care and other health news of the day. Dr. Raj is often called upon to explain and demystify complicated health topics.

Education may be tied to fewer senior moments

Elderly Americans may be stretching their brains in ways that help them stave off a decline in memory and mental function, also referred to as "cognitive decline," which leads to dementia.

The findings from two nationally representative surveys, conducted in 1993 and 2002, "support the idea that more education is protective against cognitive decline," Dr. Kenneth M. Langa told Reuters Health.

A nearly 30-percent decline in cognitive impairment occurred between the 1993 and 2002 survey, Langa, of the University of Michigan, Ann Arbor, and colleagues report. Importantly, they add, the average education level was nearly one year higher in 2002 than in 1993.

The investigators analyzed medical, lifestyle and demographic information as well as measures of memory, mental processing, knowledge, language, orientation and other indicators of cognitive function from participants in the Health and Retirement Study.

There were 7,406 subjects in the 1993 survey and 7,104 in the 2002 survey. The two groups were primarily white, 40 percent male, an average of 78 years old, and about half were living with a spouse, Langa's group reports in the journal Alzheimer's and Dementia.

The investigators identified 12.2 percent of subjects as cognitively impaired in 1993. By 2002, rates of cognitive decline dropped to 8.7 percent.

In addition to achieving more education, the 2002 respondents also reported significantly greater net worth than the 1993 respondents.

"Higher levels of wealth likely lead to more or better educational opportunities and better access to health care," Langa said in an interview with Reuters Health.

Among individuals with moderate-to-severe cognitive impairment, the researchers noted higher mortality rates in the 2002 group. This implies that education may protect the brain to a point, but once it occurs, the impairment may be more severe and carry a greater risk of death.

The researchers conclude that modest improvements in education and mental stimulation during work and leisure activities may impact public health. They add that further studies should continue to assess the link between mental stimulation and cognitive impairment.

SOURCE: Alzheimer's and Dementia, online February 20, 2008.
http://news.yahoo.com/s/nm/20080225/hl_nm/education_senior_dc

Key Step In Programmed Cell Death Discovered

Investigators at St. Jude Children's Research Hospital have discovered a dance of proteins that protects certain cells from undergoing apoptosis, also known as programmed cell death. Understanding the fine points of apoptosis is important to researchers seeking ways to control this process.

In a series of experiments, St. Jude researchers found that if any one of three molecules is missing, certain cells lose the ability to protect themselves from apoptosis. A report on this work appears in the advance online publication of Nature.

"This is probably the first description of what is happening mechanistically that contributes to the ability of cells to delay apoptosis," said James Ihle, Ph.D., the paper's senior author and chair of the St. Jude Department of Biochemistry. "It provides incredible insights into how three proteins work and how they can control apoptosis."

The molecular interactions that St. Jude researchers describe in Nature play out in nerve cells and blood cells that develop from hematopoietic (blood-forming) stem cells.

A research team elsewhere recently reported that Kostmann's syndrome, a potentially fatal inherited deficiency of granulocytes in children, caused by excessive apoptosis of granulocytes, results from a deficiency in one of the three proteins, called Hax1.

"This suggests that the protein is playing basically the same role in humans as we described in mice," Ihle said.

Apoptosis rids the body of faulty or unneeded cells. However, molecular malfunctions that trigger apoptosis may cause some diseases, including Parkinson's disease. Understanding the biochemical interactions that control the extent of programmed cell death could lead to new treatments.

St. Jude biochemists have long studied how cytokines--small proteins used by neurons and blood-borne cells to communicate messages--contribute to keeping cells alive. For example, they demonstrated earlier that most cytokines controlling hematopoietic cells require an enzyme called Jak2, or Jak3 in lymphocytes, at the receptors where cytokines attached to the cell.

In screening for components that are regulated by the Jak enzymes, the St. Jude team found the Hax1 protein.

"That was intriguing because several studies suggested that Hax1 was controlled by cytokine signaling," Ihle said. "Also, studies have suggested that if you overexpressed Hax1 in cells, the cells were protected from undergoing apoptosis."

To pursue this lead, the researchers genetically engineered mice that lacked the gene for Hax1. The results showed that apoptosis in the animals' brain caused extensive nerve cell degeneration that killed the mice within 10 to 12 weeks. Second, apoptosis in immune-system lymphocytes occurred in the altered mice eight hours sooner than in those with the Hax1 gene, when limited amounts of cytokines were available.

"That additional window of survival is extremely important because in the body, cytokines are limiting." Ihle said. "The key observation was that Hax1 was important in helping cells to survive. Importantly, what happened to the mice we generated was remarkably similar to what happens if you remove the mitochondrial enzymes called HtrA2 or Parl."

Exploring the similarities, the investigators found that Hax1 and Parl pair up in the inner membrane of the mitochondria--tiny chemical packets that serve as the main energy source for cells. HtrA2 is made in the cell's cytoplasm and is transported into the mitochondria, where the enzyme must have a region removed for it to be active. This requires snipping away 133 amino acids, the building blocks of proteins. The St. Jude researchers demonstrated that it is the Hax1/Parl pair that positions HtrA2 to allow the precise snipping that is required. Without Hax1, the snipping does not occur and HtrA2 remains inert.

In lymphocytes, members of the Bcl-2 family of proteins both protect and initiate apoptosis. For this reason, Ihle and the researchers explored this family of proteins to understand why lymphocytes needed an active HtrA2 mitochondrial enzyme. This led them to discover that if active HtrA2 were present, the incorporation of a protein called Bax into the mitochondrial outer membrane did not occur. This was significant since accumulation of Bax in the outer mitochondrial membrane allows the release of proteins that set off a chain of biochemical reactions, including the activation of enzymes that are responsible for cell death.

Other authors of this study include Jyh-Rong Chao, Kelli Boyd, Evan Parganas, Cheol Yi Hong and Joseph T. Opferman (all St. Jude).

This work was supported in part by grants from the National Institutes of Health and ALSAC.
http://www.sciencedaily.com/releases/2008/02/080229141831.htm

Study: Being fit can lower stroke risk

Being merely moderately fit — walking briskly half an hour a day — can lower the risk of having a stroke, according to a new study whose findings apply to women as well as men.

Much of the previous research on stroke and fitness has been on men and relied on participants to report their physical activity, said Steven Hooker, who heads the University of South Carolina's Prevention Research Center in Columbia and led the study. About a quarter of those in the new study were women, and everyone had a treadmill test to measure his or her fitness level.

"It seems that benefits we've been observing in men for many years ... are also observed in women," Hooker said.

He said even those who were moderately fit had a lower risk of stroke. Most people can reach that fitness range by walking briskly for 30 minutes a day, five times a week, said Hooker, who presented the findings Thursday at the International Stroke Conference in New Orleans.

Stroke is the nation's third-leading cause of death. It occurs when blood flow to the brain is stopped when a blood vessel is blocked by a clot or bursts. Hooker said physical activity can help prevent blood clots and the buildup of artery-clogging plaque.

For their research, Hooker and his colleagues used data from a study of more than 61,000 adults at the Cooper Aerobics Center in Dallas. After taking a treadmill test, the participants periodically answered health surveys. The latest research divided the group into four levels of fitness and looked at how many of them had strokes, following them an average of 18 years.

Overall, there were 692 strokes in men and 171 in women.

The study found that men in the most fit group had a 40 percent lower risk of stroke than the least fit men. The most fit women had a 43 percent reduction in their risk of stroke compared with women in the least fit group.

For moderate levels of fitness, the risk reduction ranged from 15 to 30 percent for men and 23 to 57 percent in women.

The lower risks held true even when taking into account other risk factors for stroke such as smoking, weight, high blood pressure, diabetes and family history.

Fitness is "a strong predictor of stroke risk all by itself," Hooker said.

The study's participants were mostly white, well-educated and middle-income or higher; other populations should be studied, he said. Fitness tests were only done when people entered the study so the researchers didn't know if their fitness level changed over time.

In its stroke prevention guidelines, the American Stroke Association recommends at least 30 minutes of physical activity of moderate intensity on most days of the week. The new study "is certainly consistent with all of the recommendations that we already have in place," said Dr. Larry Goldstein, a spokesman for the group and director of the Stroke Center at Duke University.

http://news.yahoo.com/s/ap/20080222/ap_on_he_me/fitness_stroke

Starved for Sleep? Watch Your Waistline

(HealthDay News) -- Could the key to weight loss for some people be as simple as getting some extra shuteye?

Possibly. New research suggests that people who don't get enough sleep tend to weigh more -- and that sleep can affect levels of the appetite-regulating hormones leptin and ghrelin.

"There is a dynamic balance between proper sleep and proper health. Sleep deprivation affects weight and a lot of other things. If you cheat sleep, there are a number of consequences, including affecting your hormones, appetite and mood," said Dr. Patrick Strollo, medical director of the University of Pittsburgh Medical Center's Sleep Medicine Center.

Two out of three Americans are overweight, and almost one in five are obese, according to the U.S. Centers for Disease Control and Prevention. And, while most people are aware of the relationship of diet and exercise to excess weight, few realize that the amount of sleep they get each night can also affect their weight.

Researchers at the Sleep Disorders Center at Sentara Norfolk General Hospital in Virginia conducted two studies, each included 1,000 men and women, and they found that those who reported sleeping less tended to weigh more.

Of course, it could be that being overweight might make it harder to get a restful night sleep.

"People who are overweight may have less restful sleep due to heartburn, snoring or more serious sleep disorders like sleep apnea or night eating syndrome," said Dr. Michelle May, author of "Am I Hungry? What To Do When Diets Don't Work."

But, she said, "It works both ways," and that a lack of sleep can affect your weight. Sleep deprivation affects your body chemistry, appetite and the choices that you make throughout the day, May said.

Another recent study included 12 healthy men in their 20s. Each of the men slept only four hours for two nights. The study found that levels of leptin, a hormone that tells the brain it's time to stop eating because the stomach is full, decreased by 18 percent during the two-day study period. Levels of another hormone, ghrelin, which turns the hunger mechanism on, increased by 28 percent.

On average, the men reported that their hunger pangs increased by 24 percent.

"Hormones change with sleep loss and deprivation," said Strollo. "Sleep deprivation can affect appetite and also the type of food that one desires. When you're sleep-deprived, you generally don't crave carrot sticks."

May agreed, adding, "When you're tired, you're less resilient to stress and other common emotional triggers for eating. When you eat to help you cope with emotions, you're more likely to choose comfort foods like chocolate, ice cream or chips. And, since eating only helps temporarily, you may find yourself reaching for food again and again to try to make yourself feel better.

"Getting enough sleep is the best way to prevent sleep deprivation from contributing to weight gain," May advised. "When you aren't able to get your Zzzs, pay more attention to how much you eat and how you handle fatigue and stress. A short walk will be a better energy boost than a trip to the candy machine."

Strollo said that while most people need between seven and eight hours of sleep a night, there are some people who need as many as 10 and others who may do well on just five hours.

The best way to figure out how much sleep you need, he said, is to take a long vacation and after a couple of days of catching up on your sleep debt, see how many hours of sleep you need to wake without an alarm clock. Since many Americans don't take long vacations, if you feel that you're not fully functional all day, or that you're doing things to stay awake, like a double-espresso shot, you're probably not getting enough sleep, he said.

May added that it's important to remember that "healthy eating, physical activity and sleep are not luxuries, they are necessities."

More information

To learn more about the connection between sleep and your weight, visit the National Sleep Foundation.

Faulty Fountains of Youth

Skin sags. Hair grays. Organs don't work quite like they used to. A gradual wearing out and running down of the body's tissues seems an inherent part of growing older. Rejuvenation of skin, muscles, and other body parts naturally declines with the passing years.

Scientifically speaking, however, this observation is much less self-evident. Some cells in a person's body can resist the tide of aging. Consider the reproductive cells a person carries that will become the cells of newborn children who have 80-plus years of life to look forward to. Generation after generation, these reproductive cells form an unbroken line stretching for millennia.

The reason that an otherwise healthy person grows old and dies remains a mystery. Scientists have suggested several suspects for why people's bodies wear out with age, including accumulated damage to DNA, free radicals, and the shortening of telomeres—the caps on the ends of chromosomes. While each of these factors may play a part, biologists acknowledge that their understanding of aging is incomplete.

Enter stem cells. Scientists have long known that people have small reservoirs of stem cells in some of their tissues, such as bone marrow. These stem cells are distinct from those found in newly fertilized embryos—the more controversial embryonic stem cells. The embryonic type can become any type of cell in the body.

Adult stem cells, in contrast, can normally generate new cells only for the tissue in which they're found: blood cells for blood, intestinal cells for the intestines. As old cells in these tissues are damaged or wear out, nearby stem cells can manufacture new ones to take their place. At the same time, the stem cells produce more copies of themselves, maintaining a seemingly indefinite pool of cells capable of churning out a stream of replacement cells.

Until recently, most scientists thought that adult stem cells existed only in tissues that need to constantly replace their cells, such as skin, blood, and the lining of the intestine. But over the past few years, researchers have found stem cells in many, perhaps most, of the body's organs and tissues. Even the brain, which scientists once thought never replaced its nerve cells during adulthood, is now known to have stem cells that make new nerve cells throughout life (SN: 6/16/07, p. 376).

With the realization that so much of the body contains self-renewing stem cells, scientists began wondering whether changes in these stem cells over time might contribute to aging.

Imagine that, as a person ages, these fountains of cellular youth might start to run dry. As the supply of fresh cells dwindles, tissues would gradually decline and show signs of age. "That was the initial model" of how stem cells could be involved in aging, says Norman E. Sharpless, a stem cell expert at the University of North Carolina in Chapel Hill. And some data support this idea.

Graying of hair, for example, could be caused by a decline in melanocyte stem cells that accompanies aging, as observed by Emi K. Nishimura and her colleagues at Dana-Farber Cancer Institute in Boston. Melanocytes make the hair pigment melanin, so depleting these stem cells eventually causes loss of hair color, the team reported in Science in 2005.

Elderly people also have diminished resistance to disease because their immune systems make fewer of the disease-fighting white blood cells known as lymphocytes. In mice, bone marrow stem cells produce fewer lymphocytes as the mice get older, Derrick J. Rossi, now at Harvard Stem Cell Institute in Cambridge, reported in 2005 in the Proceedings of the National Academy of Sciences.

Yet evidence is mounting that the connection between adult stem cells and aging is more complex. Some kinds of stem cell actually grow more abundant with age. And just as stem cells affect aging, the aging body affects stem cells.
Tinkering with time

To untangle these effects, scientists led by Thomas A. Rando of Stanford University surgically joined pairs of mice like reconnected Siamese twins. The team linked the animals' circulatory systems so that blood from each member of a pair flowed through both mice. One mouse in each pair was old; the other was young.

Scientists knew that the ability of muscle stem cells (also called satellite cells) to repair damaged muscles declines substantially with age. Rando's team wanted to find out whether such declines should be attributed to changes in the satellite cells themselves or to changes in the cells' environment as the animals aged.

"There clearly is an effect of aging on stem cells," Rando says. "But I think the other question is ... are those changes reversible or irreversible?"

Amazingly, the blood of the young mice completely restored the tissue-healing powers of the satellite cells in the older mice, Rando's team reported in 2005 in Nature. Exposure to the young blood reactivated a system of proteins inside the cells called the Notch signaling pathway, which is crucial for triggering the cells' muscle-repair functions. Notch signaling in satellite cells normally declines in old age, but Rando's experiment showed that this decline is a response to changes in the blood, not the result of an inherent wearing out of the satellite cells themselves.

This influence of the cells' environment is possible because all cells receive signals—including hormones and other messenger proteins—from their surroundings, and these signals allow the cells to behave appropriately for their context. So a change in these external messengers in aging mice could diminish the satellite cells' muscle-repair activity.

Stem cells' surroundings also wield an influence in fruit fly testes. Changes in the stem cell–harboring niche inside the testes contribute to a decline in the number of sperm-making stem cells with age, according to research by D. Leanne Jones of the Salk Institute for Biological Studies in La Jolla, Calif., and her colleagues. As the flies grew old, the niche produced less of a protein that activates a gene in the stem cells called unpaired, which triggers self-renewal of the cells, the team reported in the Oct. 11, 2007 Cell Stem Cell.

"We definitely see changes in the environment long before we start to see" signs of intrinsic aging, Jones says. In mice testes as well, "there seems to be evidence for the environment aging instead of the stem cells themselves."

In other cases, though, stem cell aging seems independent of context. Blood-forming stem cells from bone marrow age in an unusual way. When scientists transplant blood stem cells from an old mouse into a young mouse, allow the young mouse to grow old, and then repeat the process for several generations, the stem cells lose none of their ability to make copies of themselves. In fact, in some mouse strains, blood stem cells become even more numerous with age.

But that's not necessarily a good thing. While old age doesn't appear to affect blood stem cells' power of self-renewal, it does gum up their ability to make specialized offspring cells. Ideally, each time a stem cell divides, one of the daughter cells would remain a stem cell, and the other would continue dividing to produce a fresh crop of specialized cells to replenish the tissue. That way, the stem cell's lineage always contains only one stem cell at a time to replace the original, keeping the total number of stem cells constant.

For that number to increase, daughter cells must sometimes both become stem cells, decreasing production of tissue-replenishing cells.

Even when these elderly stem cells do spawn new lines of specialized cells, the process goes awry. Blood stem cells must give rise to a whole family of specialized cells: red blood cells, lymphocytes, monocytes, macrophages, and others. As the stem cells age, something goes wrong in this specialization process, skewing it away from making lymphocytes. So the old-age slump in germ-fighting lymphocytes happens not because the stem cells peter out but because they charge ahead with their specialization machinery slightly broken. In mice, this misbehaving of blood stem cells occurs even when scientists repeatedly transplant the cells into young animals, leading them to conclude that the stem cells themselves become damaged with time.
Fighting death with aging

In trying to understand how stem cells in various organs deteriorate with age, scientists have run up against the perennial nemesis of cell biology: cancer.

"Having all these cells around that can divide all the time is quite dangerous for an organism," Sharpless says. Cells continually accumulate DNA damage, but copying and segregating the DNA during cell division is particularly hazardous. Every time a cell divides, there's some error of replication.

Most of these mistakes get fixed by repair enzymes, but certain lingering errors in DNA can cause a cell to begin growing and dividing out of control, which is how cancer arises. Cells have elaborate tools for detecting DNA damage early and either fixing it or shutting down the affected cell. Recent data suggest that these mechanisms for thwarting cancer could cause the body to cull some of its own stem cell supplies.

For example, researchers led by Sean J. Morrison of the University of Michigan in Ann Arbor found a link between the decline in nerve stem cells in mouse brains and the potent anticancer gene p16. This gene causes cells to enter a dormant state called senescence. Mice bred without p16 retained significantly more of their nerve stem cells into old age than did mice that had the gene, Morrison's team reported in Nature in 2006.

The famous tumor-fighting gene p53 also reins in damaged stem cells in old age. Blocking the activity of p53 in stem cells restored populations of intestinal stem cells in elderly mice, K. Lenhard Rudolph of Hannover Medical School in Germany and his colleagues reported in the January 2007 Nature Genetics.

Whether the bodily declines that come with aging are due to the depletion of stem cells depends on which organ is in question—and on which scientist you ask. Most scientists agree that adult stem cells play an important role in aging; the other thing that they seem to agree about is that this role is complicated. "There's still a tremendous amount of debate about even the [blood stem cell] system, which is one of the best-studied systems," Jones says.

In blood and other tissues with high cell turnover, decline of stem cells may make a greater contribution to the signs of aging than it does in tissues with slower cell turnover.

In skin, which constantly produces new cells, a decline in stem cell vigor is expected by some scientists to play a big part in the sagging and poor elasticity of skin that comes with old age. For organs such as the brain and heart, which retain most of their cells throughout adulthood, signs of old age more likely come from traditional mechanisms of aging acting on the organs' mature, specialized cells.

But even this guideline may be too simple. Alzheimer's disease, a form of dementia that commonly occurs in the elderly, is characterized by plaques accumulating in the brain. Young people's brains make the plaque proteins as well, but some data suggest that immune cells called macrophages patrol the brain and clear out budding plaques. Macrophages are continuously being made by—you guessed it—blood stem cells. So even for organs in which cell renewal by stem cells proceeds very slowly, the declines of old age might be caused by the decline of adult stem cells elsewhere in the body.

Some aspects of aging will likely prove unrelated to stem cells, Sharpless says, but these cells now appear far more important for aging than scientists once thought. "I've stopped trying to predict which symptoms of aging are related to [stem cell] proliferation and which are not," Sharpless says. Scientists "used to be so confident about this 10 years ago. Now I'm prepared to be wrong."



http://www.sciencenews.org/articles/20080209/bob8.asp

Study: Being fit can lower stroke risk

Being merely moderately fit — walking briskly half an hour a day — can lower the risk of having a stroke, according to a new study whose findings apply to women as well as men.

Much of the previous research on stroke and fitness has been on men and relied on participants to report their physical activity, said Steven Hooker, who heads the University of South Carolina's Prevention Research Center in Columbia and led the study.

About a quarter of those in the new study were women, and everyone had a treadmill test to measure his or her fitness level."It seems that benefits we've been observing in men for many years ... are also observed in women," Hooker said.

He said even those who were moderately fit had a lower risk of stroke. Most people can reach that fitness range by walking briskly for 30 minutes a day, five times a week, said Hooker, who presented the findings Thursday at the International Stroke Conference in New Orleans.

Stroke is the nation's third-leading cause of death. It occurs when blood flow to the brain is stopped when a blood vessel is blocked by a clot or bursts. Hooker said physical activity can help prevent blood clots and the buildup of artery-clogging plaque.

For their research, Hooker and his colleagues used data from a study of more than 61,000 adults at the Cooper Aerobics Center in Dallas. After taking a treadmill test, the participants periodically answered health surveys.

The latest research divided the group into four levels of fitness and looked at how many of them had strokes, following them an average of 18 years.Overall, there were 692 strokes in men and 171 in women.The study found that men in the most fit group had a 40 percent lower risk of stroke than the least fit men.

The most fit women had a 43 percent reduction in their risk of stroke compared with women in the least fit group.For moderate levels of fitness, the risk reduction ranged from 15 to 30 percent for men and 23 to 57 percent in women.

The lower risks held true even when taking into account other risk factors for stroke such as smoking, weight, high blood pressure, diabetes and family history.Fitness is "a strong predictor of stroke risk all by itself," Hooker said.

The study's participants were mostly white, well-educated and middle-income or higher; other populations should be studied, he said. Fitness tests were only done when people entered the study so the researchers didn't know if their fitness level changed over time.

In its stroke prevention guidelines, the American Stroke Association recommends at least 30 minutes of physical activity of moderate intensity on most days of the week.

The new study "is certainly consistent with all of the recommendations that we already have in place," said Dr. Larry Goldstein, a spokesman for the group and director of the Stroke Center at Duke University.

http://news.yahoo.com/s/ap/20080222/ap_on_he_me/fitness_stroke

Computers 'spot Alzheimer's fast'

Computers can diagnose Alzheimer's disease faster and more accurately than experts, research suggests.

University College London researchers say their work may help ensure patients are diagnosed earlier, increasing the chances of effective treatment.

Their study, published in the journal Brain, found computers can identify brain damage caused by Alzheimer's with an accuracy as high as 96%.

At present a definitive diagnosis is usually only possible after death.

Alzheimer's is caused by the build up in the brain of plaques and tangles of brain tissue filaments, which causes tissue to start wasting away.

It is currently diagnosed using a combination of brain scans, blood tests and patient interviews, but distinguishing the disease from other forms of dementia is difficult, and time consuming, and the accuracy of diagnosis is only about 85%.

The new method works by teaching a standard computer the differences between brain scans from patients with proven Alzheimer's, and people with no signs of the disease.

The two conditions can be distinguished with a high degree of accuracy on a single clinical MRI scan.

Researcher Professor Richard Frackowiak said: "The advantage of using computers is that they prove cheaper, faster and more accurate than the current method of diagnosis.

"The new method makes an objective diagnosis without the need for human intervention.
"This will be particularly attractive for areas of the world where there is a shortage of trained clinicians and when a standardised reliable diagnosis is needed, for example in drug trials."

Speed important

Professor Frackowiak emphasised that as symptoms only emerge after a considerable amount of damage has already occurred in the brain it is important to make an accurate diagnosis early to improve the chances of effectively preventing further deterioration.

He said: "The next step is to see whether we can use the technique to reliably track progression of the disease in a patient.

"This could prove a powerful and non-invasive tool for screening the efficacy of new drug treatments speedily, without a need for large costly clinical trials."

Dr Susanne Sorensen, of the Alzheimer's Society, said: "Currently, MRI imaging is not routinely used in diagnosing the diseases causing dementia.

"This paper puts a strong case for the wider use of this technique."

Dr Sorensen said it was vital the National Dementia Strategy currently being produced by the government makes early diagnosis a high priority.

Rebecca Wood, of the Alzheimer's Research Trust, said: "This promising computer aided technique could act as a second opinion to increase the accuracy of a doctor?s diagnosis.
"However, this research is in the early stages and further analysis is required to understand the full benefits and accuracy of this technique and to see if it can be used to assess the effectiveness of new drugs."

It is estimated that over 700,000 people in the UK are currently living with dementia, of which Alzheimer's is the most common form.

http://news.bbc.co.uk/1/hi/health/7258379.stm

Strokes among middle-aged women triple

Strokes have tripled in recent years among middle-aged women in the U.S., an alarming trend doctors blame on the obesity epidemic. Nearly 2 percent of women ages 35 to 54 reported suffering a stroke in the most recent federal health survey, from 1999 to 2004. Only about half a percent did in the previous survey, from 1988 to 1994.

The percentage is small because most strokes occur in older people. But the sudden spike in middle age and the reasons behind it are ominous, doctors said in research presented Wednesday at a medical conference.

It happened even though more women in the recent survey were on medicines to control their cholesterol and blood pressure — steps that lower the risk of stroke.Women's waistlines are nearly two inches bigger than they were a decade earlier, and that bulge corresponds with the increase in strokes, researchers said.

In addition, women's average body mass index, a commonly used measure of obesity, rose from 27 in the earlier survey to 29. They also had higher blood sugar levels.No other traditional risk factors like smoking, heart disease or diabetes changed enough between the two surveys to account for the increase in strokes.

In a "pre-stroke population" of middle-age women, a tripling of cases is "an alarming increase," said Dr. Ralph Sacco, neurology chief at the University of Miami Miller School of Medicine.The study was led by Dr. Amytis Towfighi, a neurology specialist at the University of Southern California in Los Angeles, and presented at the International Stroke Conference in New Orleans.

She used the National Health and Nutrition Surveys, a federally funded project that gives periodic health checkups and questionnaires to a wide sample of Americans. Participants are routinely asked whether a doctor had ever told them they had had a stroke, and about 5,000 middle-aged people answered that question in each survey.

Researchers saw that the stroke rate had spiked in middle-aged women but stayed about the same — around 1 percent — in middle-aged men. So they looked deeper at the responses to see if they could learn why.Belly fat stood out, Towfighi said. The portion of women with abdominal obesity rose from 47 percent in the earlier survey to 59 percent in the recent one.

The change in men was smaller, and previous studies have shown that "abdominal obesity is a stronger risk factor for women than men," she said.Men traditionally have had a greater risk of stroke than women, and "women start catching up to men five or 10 years after menopause," said Dr. Philip Gorelick, neurology chief at the University of Illinois in Chicago and chairman of the stroke conference.

The new research means "we need to redefine our textbooks about stroke in women," because they may now be more at risk in middle age than men.Obesity "sets the stage for all the other risk factors to come in" like diabetes and heart disease, Gorelick added.In other news at the conference, two studies found that stroke patients were more likely to die if they went to hospitals on nights or weekends, echoing other recent studies that found similar risks for heart attack and surgery patients.

Michigan State University doctors analyzed 222,500 stroke cases at more than 850 hospitals participating in an American Heart Association quality improvement program from 2003 to 2007.In-hospital deaths were about 6 percent for those who arrived during normal business hours and had strokes caused by a clot, compared with 5 percent of those who entered the hospital after-hours. Deaths were 27 percent for off-hour strokes caused by bleeding in the brain versus 24 percent during normal hours.

A second study of 2.4 million stroke patients in California found death rates of 10 percent on weekends and nights versus 8 percent during weekdays.Despite the poorer outcomes, doctors said no one should ever delay getting help, since any delay raises the risk of death. The best treatments can only be given in the first few hours after symptoms appear.

http://news.yahoo.com/s/ap/20080221/ap_on_he_me/obesity_strokes

Brain drug target discovery in MS

US researchers have found two potential targets for treating multiple sclerosis after an extensive trawl through proteins in the brain.

Comparison of 2,538 proteins from MS patients with those from healthy brains showed damage in two proteins not before linked to the disease.

In mice blocking the effects of the proteins led to reversal of symptoms, the study in Nature reported.

There are about 85,000 people with MS in the UK.

The condition is caused by a defect in the body's immune system, which turns in on itself, attacking the fatty myelin sheath which coats the nerves, leading to symptoms including blurred vision, loss of balance and, in some cases, paralysis.

Study leader Professor Lawrence Steinman said this was the first large-scale study to search for defective proteins in MS lesions in the brain.

They found a few proteins peculiar to MS brain lesions.

But two in particular - tissue factor and protein C inhibitor - showed signs of damage during the chronic active stage of the disease.

These normally participate in the control of blood clotting and in anti-inflammatory pathways. The researchers guessed that the damaged proteins might be helping the progression of MS and, by using inhibitors of the proteins found they could successfully ameliorate the disease in mice.

Treatment

Professor Steinman, from Stanford University School of Medicine in California, said the finding opened up the way for new treatments.

However, using existing drugs which interfere with the control of blood clotting would be dangerous because of an increased risk of bleeding.

Professor Neil Scolding, from the University of Bristol Institute of Clinical Neurosciences, said: "From the scientific perspective, the exciting thing is that it's pretty much the first time that proteomics has directly yielded a candidate molecule that is both unexpected and novel on the one hand and has therapeutic potential.

"From the clinical perspective, showing that treatment approaches predicted by this proteomic interrogation of MS tissue do have a clear impact in experimental models of MS is extremely promising.

"This points the way to a new area of MS research of considerable interest, and which could well lead in the future to new lines of treatment."

Dr Laura Bell, Research Communications Officer at the MS Society, said she looked forward to seeing how the research progressed.

"This is early research but provides an interesting insight into some of the potential players that cause different types of damage to the central nervous system in people with MS.

"Understanding how MS develops is vital to target therapies for the condition."

http://news.bbc.co.uk/2/hi/health/7247420.stm