New look at Alzheimer's approach

Scientists have revealed that Neuro-Fibrillary Tangles - known as Tau - are more likely to be an effect of Alzheimer's disease rather than a cause, it has been noted. ... Continue Reading

Daily pill that halts Alzheimer's is hailed as 'biggest breakthrough against disease for 100 years'

A new drug halts the devastating progress of Alzheimer's disease, say British scientists. ... Continue Reading

Alzheimer's drug may treat memory loss

A study looking into the long-term impact of a drug created to help sufferers of Alzheimer's disease has concluded that it may aid memory loss. ... 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

Antihistamine drug proven effective in treating Alzheimer's

A drug previously approved as an antihistamine in Russia may serve as a potential treatment for Alzheimer's disease, new findings indicate. ... Continue Reading

Men 'more likely' to encounter cognitive problems as they age

Cognitive impairment associated with aging, such as memory problems and early signs of dementia seems to affect older men more than older women, according to scientists in the US.

Research conducted at the Mayo Clinic in Rochester, Minnesota, found that men were 1.6 times more likely to have mild cognitive impairment than women, regardless of education or marital status.

Commenting on the study, research co-investigator Dr Rosebud Roberts, associate professor of epidemiology at the Mayo Clinic and member of the American Academy of Neurology, said: "This is one of the first studies to determine the prevalence of mild cognitive impairment among men and women who have been randomly selected from a community to participate in the study."

In an attempt to offer an explanation for the findings, she suggested that maybe "there's a delayed progression to dementia in men or women may develop dementia at a faster rate than men".

The Alzheimer's Association recommends older people maintain a rich social and physically active lifestyle in addition to following a low-fat, low-cholesterol diet.

Antipsychotic Drugs of Little Benefit to Alzheimer's Patients

, (HealthDay News) -- The continuing use of antipsychotic drugs provides no cognitive or neuropsychiatric benefit for Alzheimer's patients, a British study concludes.

Researchers at King's College Hospital in London studied 165 patients who were already being treated with antipsychotic drugs. The patients were divided into two groups -- one continued treatment with the drugs, while the other group stopped treatment.

The patients were assessed six and 12 months later, and the researchers found no differences between the two groups in terms of cognitive decline or in the number of neuropsychiatric problems.

Patients with severe neuropsychiatric problems at the start of the study may have derived some benefit from continued drug therapy, but this difference was not statistically significant, the researchers said.

While these findings suggest that continued use of antipsychotic drugs offers no benefits for Alzheimer's patients, this was a small study, the study authors noted. More research is needed to improve management of these patients, they added.

The study appears in the cuurent issue of PLoS Medicine.

Almost all older dementia patients have some neuropsychiatric symptoms, such as agitation, aggression and psychosis. Antipsychotics are often used to manage or control these symptoms, but there are safety concerns, including increased risk of stroke, sedation, edema, chest infections and parkinsonism. Prolonged use of antipsychotics may also lead to a worsening of cognitive decline.

More information
The U.S. National Institute on Aging has more about Alzheimer's medications.

'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

Gene Linked to Form of Parkinson's Disease

(HealthDay News) -- Mutations in a gene called GIGYF2 may be directly linked to the development of Parkinson's disease in families with a history of the neurodegenerative condition, U.S. researchers report.

"These findings may ultimately help open the door to the development of new therapeutic -- and possibly even preventive -- strategies that target the underlying cause of Parkinson's disease, improving quality of life of the many people worldwide who are affected by this devastating disorder," senior author Dr. Robert J. Smith, professor of medicine at the Warren Alpert Medical School of Brown University, said in a prepared statement.

His team analyzed DNA samples from 249 Parkinson's patients with at least one first-degree relative (parent, child, sibling) with the disease, and compared them to DNA samples from 200 healthy people.

The researchers found that GIGYF2 resides on a chromosomal region called PARK11, which is linked to Parkinson's.

"Our data provides strong support for GIGYF2 as a PARK11 gene with a causal role in familial Parkinson's disease," said Smith, who is also director of the division of endocrinology and the Hallett Center for Diabetes and Endocrinology at Rhode Island Hospital.

"The next step is to zero in on this gene to learn more about its involvement in triggering Parkinson's. It will also be important to evaluate additional and larger families with Parkinson's and these genetic mutations, as well as the frequency of GIGYF2 mutations in patients with the more common, idiopathic form of the disease," he said.

The study appears online in the American Journal of Human Genetics and will be published in the April 11 print issue of the journal.

Smith and his colleagues said GIGYF2 is one of only a few genes so far linked to Parkinson's and one of just two genes known to be a common contributor to the disease, which has no known cause or cure and affects as many as one million Americans.

They noted that less than one-quarter of all Parkinson's cases are familial. But findings about genes like GIGYF2 could improve understanding of the mechanisms behind Parkinson's and may help lead to new treatments for all forms of the disease, the researchers said.

They also identified a possible association between Parkinson's and insulin and the related growth hormone called insulin-like growth factor (IGF). This adds to a growing body of research linking insulin and IGF to Parkinson's, Alzheimer's and other neurodegenerative diseases.

"A better understanding of the link between insulin or IGF and Parkinson's may lead us to new treatment strategies for Parkinson's and also new insights into the connection between diabetes and nervous system disorders," Smith said.

More information
We Move has more about Parkinson's disease.

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

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

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