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(Health) Aging: Fountain of Youth within Reach?
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PostPosted: Sun Feb 19, 2006 7:42 am    Post subject: (Health) Aging: Fountain of Youth within Reach? Reply with quote






Fountain of youth within reach?
By CHRISTINE DELL'AMORE
ST. LOUIS, Feb. 17 (UPI) -- The day when people retire at 85 and live well into their 100s may be on the horizon, thanks to promising research in anti-aging therapies, researchers said Friday.

In animal studies over the past 15 years, scientists have found that restricting the caloric intake of animals and mutating certain genes slows the aging process and makes them live longer.

"We've been wildly successful in extending life and improving health of a variety of animals. It has made even those of us who are skeptical think it might pan out with humans," said Steven Austad, a biologist at the University of Texas Health Science Center. However, Austad added that such therapies have side effects in animals, such as a higher susceptibility to infectious diseases. "This strikes me as a critically important issue that has been ignored," he said.

He discussed the research on a panel on anti-aging and its possible social costs at the American Association for the Advancement of Science meeting in St. Louis.

There is a considerable chance that, in the next two decades, anti-aging therapy could increase a middle-aged person's life by 20 years, said Aubrey de Grey, a biomedical gerontologist at the University of Cambridge in England. Likewise, between 2010 and 2030, the age of death may rise an average of 20 years if anti-aging therapies are applied.

But challenges to society might temper such advances. For one thing, the developing world would likely not benefit from anti-aging drugs; many in Africa still struggle with getting basic HIV medicine, said Shripad Tuljapurkar, a demographer at Stanford University.

In the United States, there are two retired people for every five in the workplace, and this could explode to four for every five people, sparking unprecedented problems for healthcare and other infrastructures, he said.

For example, Social Security would be overburdened, particularly because of the "intrinsic assumption" that people work and enjoy retirement. The big question is how people will pay for an additional 30 years of life, Tuljapurkar said. "Never in history have we had a population where the median age is 50, and it might happen in 30 or 40 years," he said.

Demographer Eileen Crimmins of the University of Southern California told UPI that the answer may be as simple as upping the retirement age. She said society will adjust to the boom in older people, just as people have already adjusted to longer lives by delaying adulthood and marrying more than once. It boils down to a question of social values, not demographics, she said.

"They will not be anything we can't deal with using sensible policies," she said.

De Grey emphasized that he and other anti-aging scientists are not focused on extending life, but slowing aging. Extending life without addressing aging could be a train wreck for society, with millions of people suffering from Alzheimer's and other degenerative conditions of aging, Austad said.

A longer life is just a side benefit to preventing diseases such as arthritis and cataracts and improving the functionality of the body, de Grey said.

De Grey is an expert in a controversial area that says aging can be delayed indefinitely by using a repair and rejuvenate strategy. He sees the human body as a house, which needs consistent maintenance to stay structurally sound. If seven key operations of the body can be stopped -- among those, the death of cells, accumulation of toxic cells and accumulation of damage to the DNA -- a person's health can be continually maintained. "Since we didn't design our own anatomy, we just need to figure out how to do it," he said.

Still, de Grey and anti-aging therapy has been met with stiff resistance.

De Grey told UPI that this resistance is symptomatic of a "pro-aging trance," and that Americans do not see aging for the ghastly process that it is.

"We're making ludicrous excuses for aging that we never use for heart disease," de Grey said. "But there are no reasons [against anti-aging] that can outweigh 100,000 people lost a day."

*************************************************************

Questions to explore further this topic:

What is aging?

http://www.trinity.edu/~mkearl/ger-biol.html
http://www.sportsci.org/encyc/agingex/agingex.html
http://www.basis.ncl.ac.uk/biology.html

The Biology of Aging (A High School Lesson Plan)

http://fi.edu/guide/sowd/intro.html
http://www.sciencenetlinks.com.....;DocID=191
http://www.sciencenetlinks.com.....?DocID=200

The Biology of Aging (A powerpoint presentation)

http://users.ipfw.edu/Blumenth.....tation.PDF

The Science of Aging (Audio and Visual Presentation)

http://www.pbs.org/newshour/bb....._2-28.html

What is our image of aging?

http://library.thinkquest.org/.....image.html
http://library.thinkquest.org/.....unity.html

What is the cellular basis of aging?

http://library.thinkquest.org/.....lular.html

Oxidative damage
http://websites.afar.org/site/.....oxdam_home

Telomeres
http://websites.afar.org/site/.....b_tel_home

DNA damage
http://websites.afar.org/site/.....b_dna_home

Mitochondrial aging
http://websites.afar.org/site/....._mito_home

Cellular senescence
http://websites.afar.org/site/....._sene_home

What changes occur with aging?

Organs, Tissues and Cells
http://www.nlm.nih.gov/medline.....004012.htm

Hormone production
http://www.nlm.nih.gov/medline.....004000.htm

Immunity
http://www.nlm.nih.gov/medline.....004008.htm

Skin
http://www.nlm.nih.gov/medline.....004014.htm

Sleep
http://www.nlm.nih.gov/medline.....004018.htm

Bones. Muscles and Joints
http://www.nlm.nih.gov/medline.....004015.htm

Breast
http://www.nlm.nih.gov/medline.....003999.htm

Face
http://www.nlm.nih.gov/medline.....004004.htm

Female reproductive system
http://www.nlm.nih.gov/medline.....004016.htm

Male reproductive system
http://www.nlm.nih.gov/medline.....004017.htm

Heart and Blodd Vessels
http://www.nlm.nih.gov/medline.....004006.htm

Kidneys
http://www.nlm.nih.gov/medline.....004010.htm

Lungs
http://www.nlm.nih.gov/medline.....004011.htm

Nervous system
http://www.nlm.nih.gov/medline.....004023.htm
http://faculty.washington.edu/chudler/aging.html
http://faculty.washington.edu/chudler/ninety.html
http://faculty.washington.edu/chudler/gould.html

Senses
http://www.nlm.nih.gov/medline.....004013.htm

Vital signs
http://www.nlm.nih.gov/medline.....004019.htm

What chemistry may be involved in aging?

http://www.brown.edu/Administr.....3-149.html
http://www.bioteach.ubc.ca/Mol.....index.html
http://www.nyas.org/annals/detail.asp?annalID=820
http://www.annalsnyas.org/cgi/...../959/1/360
http://www.pbs.org/newshour/sc.....ended.html
http://www.pbs.org/newshour/fo.....intro.html

What are the current global statistics on aging?

http://www.aarp.org/research/international/map/
http://library.thinkquest.org/.....aging.html
http://library.thinkquest.org/.....tancy.html
http://library.thinkquest.org/.....round.html
http://library.thinkquest.org/.....uring.html
http://library.thinkquest.org/.....elop1.html
http://library.thinkquest.org/.....ural1.html
http://library.thinkquest.org/.....rban1.html

What challenges do developing countries face with aging?

http://library.thinkquest.org/.....orrow.html

What demand does an aging population require?

http://www.aarp.org/research/i.....index.html

GAMES

http://faculty.washington.edu/.....emory.html
http://library.thinkquest.org/.....ities.html
http://www.puzzle.dse.nl/index_us.html
http://www.brainbashers.com/
http://www.brainconnection.com/teasers/


Last edited by adedios on Sat Jan 27, 2007 4:41 pm; edited 2 times in total
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PostPosted: Mon Mar 27, 2006 7:06 am    Post subject: Older people with stronger cognitive skills walk at a safer Reply with quote

American Psychological Association
26 March 2006

Older people with stronger cognitive skills walk at a safer pace

Psychologists wanting to help old people safely cross the street and otherwise ambulate around this busy world have found that from age 70 and up, safe walking may require solid "executive control" (which includes attention) and memory skills. For the old, slow gait is a significant risk factor for falls, many of which result in disabling fractures, loss of independence or even death. The finding may help explain why cognitive problems in old age, including dementia, are associated with falls. Cognitive tests could help doctors assess risk for falls; conversely, slow gait could alert them to check for cognitive impairment. The findings are in the March issue of Neuropsychology, which is published by the American Psychological Association (APA).
Roee Holtzer, PhD, and his colleagues conducted a cross-sectional study of 186 cognitively normal, community-dwelling adults aged 70 and older at New York City's Albert Einstein College of Medicine. Gait speed was tested with and without interference. In the interference conditions, participants had to walk while reciting alternate letters of the alphabet.

Performance on cognitive tests of executive control and memory, and to a lesser extent of verbal ability, predicted "gait velocity" (walking speed) tested without interference. For gait velocity tested with interference, only executive control and memory were predictive. Adding interference to the tests of gait allowed the researchers to better simulate the real world, in which walkers continually deal with distractions. The authors conclude that executive control and memory function are important when the individual has to walk in a busy environment.

The findings suggest that in old age, walking involves higher-order executive-control processes. That is, the intersecting cognitive and motor processes involved in walking may both rely on a common brain substrate, or set of structures. As a result, changes in that substrate would affect both cognition and gait.

Falls are a serious public-health issue for an aging population. Many older people are aging in the suburbs, where traffic conditions are often not designed for pedestrians of any age. And in cities, traffic lights at busy intersections are not usually timed to give people with slower perceptions and reflexes more time to safely cross the street.

Holtzer says that risk assessment and prevention programs for falls, which have typically focused on balance, strength and gait but not cognitive function, have had limited success. Given the new research, he posits that cognitive and neuropsychological performance, plus gait, could both factor into risk assessment and intervention design. What's more, cognitive rehabilitation and/or medication targeting cognitive functions such as executive control and memory might, among other benefits, reduce the risk of falling in people at risk.

Future study is needed to follow people through the life span to see how age affects the relationship between cognitive functions and gait. Holtzer cites evidence that gait is more automatic and less effortful in young than old people and points out that even within the narrow age range of his study's participant sample, each additional year tightened the relationship between cognitive function and gait velocity.


###
Article: "Cognitive Processes Related to Gait Velocity: Results From the Einstein Again Study," Roee Holtzer, PhD, Joe Verghese, MD, Xiaonan Xue, PhD, and Richard B. Lipton, MD, Albert Einstein College of Medicine, Yeshiva University. Neuropsychology, Vol. 20, No. 2.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/releases/neu202-holtzer.pdf.)

Roee Holtzer can be reached by email at rholtzer@aecom.yu.edu or by phone at (718) 430-3962.

The American Psychological Association (APA), in Washington, DC, is the largest scientific and professional organization representing psychology in the United States and is the world's largest association of psychologists. APA's membership includes more than 150,000 researchers, educators, clinicians, consultants and students. Through its divisions in 54 subfields of psychology and affiliations with 60 state, territorial and Canadian provincial associations, APA works to advance psychology as a science, as a profession and as a means of promoting human welfare.
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PostPosted: Mon May 08, 2006 6:43 pm    Post subject: Cutting calories slightly can reduce aging damage Reply with quote

University of Florida
8 May 2006

Cutting calories slightly can reduce aging damage

GAINESVILLE, Fla., - A lifelong habit of trimming just a few calories from the daily diet can do more than slim the waistline - a new study shows it may help lessen the effects of aging.
Scientists from the University of Florida's Institute on Aging have found that eating a little less food and exercising a little more over a lifespan can reduce or even reverse aging-related cell and organ damage in rats.

The discovery, described this month in the journal Antioxidants and Redox Signaling, builds on recent research in animals and humans that has shown a more drastic 20 percent to 40 percent cut in calories slows aging damage. The UF findings indicate even small reductions in calories could have big effects on health and shed light on the molecular process responsible for the phenomenon, which until now has been poorly understood.

"This finding suggests that even slight moderation in intake of calories and a moderate exercise program is beneficial to a key organ such as the liver, which shows significant signs of dysfunction in the aging process," said Christiaan Leeuwenburgh, Ph.D., an associate professor of aging and geriatric research at the UF College of Medicine and the paper's senior author.

UF scientists found that feeding rats just 8 percent fewer calories a day and moderately increasing the animals' activity extended their average lifespan and significantly overturned the negative effects of cellular aging on liver function and overall health.

An 8 percent reduction is the equivalent of a few hundred calories in an average human diet and moderate exercise is equivalent to taking a short walk.

To reveal the workings of the body's chemical climate when aging-related damage happens, UF researchers tracked levels of biomarkers - chemicals and molecules present in the liver - in groups of rats. The liver, a crucial organ for maintaining good health during aging, cleans the blood and helps regulate the body's immune system. The researchers also plan to assess the same biomarkers in a study of rats' hearts, muscle and brains.

The research team was surprised to find one of the biomarkers, RNA, which is important for coding DNA and for protein synthesis, is more quickly damaged by aging than the more frequently studied DNA. RNA damage, therefore, could be an excellent early signal to indicate the onset of aging, researchers say.

"Because it is more sensitive to oxidative stress, RNA can be useful as an early marker of oxidative damage and even aging," said Arnold Y. Seo, a doctoral student in UF's Institute on Aging.

Seo authored the report along with Tim Hofer, Ph.D., an Institute on Aging research associate.

"To avoid disease, we can increase our defense and look for aging biomarkers and then test interventions," Hofer said. "It is better to protect what is there to improve the quality of life than to have to resort to invasive procedures."

In the study, which followed the rats over their lifespan, one group of animals ate as much food as they wanted and did not exercise, another group of animals exercised lightly and were fed slightly less than they would have eaten if allowed to have their fill. Liver samples from these groups were compared with samples taken from young rats.

The old sedentary rats that ate until they were full had increased levels of harmful oxidizing and inflammatory molecules in the liver that were associated with cell damage caused by aging. Meanwhile, aging rats that exercised and consumed a calorie-restricted diet, had the reverse outcome - they showed a decrease in these molecules in the liver.

Leeuwenburgh said the study results support the theory that cell death and aging-related organ damage are caused by unstable molecules known as free radicals and by cellular oxidation and inflammation.

"In a calorie-restricted environment, you reduce the inflammatory response and prevent cell death," Leeuwenburgh said.

John O. Holloszy, a professor of medicine in the division of geriatrics and nutritional sciences at Washington University School of Medicine in St. Louis, said the study is of major importance because it shows a mild degree of caloric restriction - just enough to prevent weight gain with advancing age - can have beneficial effects against aging. From a scientific perspective, he added, it is important to learn that RNA is a very good marker of aging damage.

"I'd never really thought about RNA before," Holloszy said. "Research has always looked at DNA. Because RNA is the template for the information on the genes on the DNA, RNA damage is a major problem because it results in mutations in the transcription of proteins."


###
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PostPosted: Thu Jun 01, 2006 1:43 pm    Post subject: Worm links cancer risk to ageing Reply with quote

University of Manchester
1 June 2006

Worm links cancer risk to ageing

The reason why people are at greater risk of developing cancer as they get older may be explained by research published today (June 2).
Scientists have discovered that a naturally produced protein that helps protect us from cancer may also determine how long we live.

The findings – published in the highly respected journal Science – open up a new avenue of inquiry into ageing as a risk factor for cancer.

"We have discovered that proteins that prevent cancer in humans by ensuring that cells don't divide if they are damaged also determine lifespan in the nematode worm," explained Professor Gordon Lithgow, who carried out the work at The University of Manchester.

"Our research has shown that these 'checkpoint proteins' – thought only to operate in cells that divide – function in cells that no longer divide as well. The fact that they appear to have dual functions opens a new way to study the connection between ageing and cancer."

Scientists have long known that, statistically, ageing is a huge factor for cancer but have so far struggled to understand why that is.

Professor Lithgow said: "If we look at checkpoint proteins as a gear, we have known for a long time that they drive the cancer engine; now we know that they also drive the longevity engine. This discovery has exciting potential as an area of inquiry into potential cellular links between ageing and cancer."

The research, which was completed at the Buck Institute in California where Dr Lithgow now works, involved genetically removing checkpoint proteins in the microscopic worm C. elegans. By doing so, the researchers caused a 15-30% increase in the worm's lifespan.

"Given the role that checkpoint proteins play in the development of cancer – or in causing tumours when the proteins are defective – the findings raise the question of whether genetic variations in these proteins in humans places some individuals at risk of cancer.

"Conversely, the checkpoint proteins may set a genetic course for a shorter life but one that is free from cancer."

Dr Dale Bredesen, Chief Executive and Scientific Director at the Buck Institute, added: "This work brings a new richness and sophistication to the way we think about longevity interventions.

"If we're smart about it, we might be able to design strategies where you could keep checkpoint proteins active in dividing cells and stop them working in cells that no longer divide, such as brain cells.

"Increasing the survival of brain cells or 'neurons' could provide a new avenue of treatment for neurodegenerative diseases like Alzheimer's."
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PostPosted: Mon Sep 18, 2006 5:04 pm    Post subject: Life is a Devil's Bargain: Cancer or Aging Reply with quote

Life is a Devil's Bargain: Cancer or Aging

By Ker Than
LiveScience Staff Writer
posted: 18 September 2006
09:33 am ET



Deterioration of body and mind are the prices our bodies pay for protection against cancer as we grow older, new studies suggest.

Scientists have discovered that a gene involved in tumor suppression also plays an important role in determining when certain cells in the body cease multiplying and start deteriorating. As cells age, the gene, called p16INK4a, becomes more active. The cells have greater protection against cancer but lose the ability to divide. Cells that don't divide die off and are not replaced.

The studies, detailed together in the Sept. 7 issue of the journal Nature, suggest the physical and mental ravages that accompany aging are not the result of simple wear and tear of the body, but of a cellular decline that is programmed into our genes—one designed to safeguard us against copying mistakes that become more frequent as we grow older.

"This research tells us why our old tissues have less regenerative capacity than young tissues," said Sean Morrison of the University of Michigan, who was involved in one of the studies. "It's not that old tissues wear out—they're actively shutting themselves down, probably to avoid turning into cancer cells."


For the full article:

http://www.livescience.com/hum.....aging.html
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PostPosted: Sun Oct 01, 2006 8:39 pm    Post subject: Osteoarthritis may be sign of faster 'biological ageing' Reply with quote

BMJ Specialty Journals
1 October 2006

Osteoarthritis may be sign of faster 'biological ageing'

Reduction of leucocyte telomere length in radiographic hand osteoarthritis: A population based study
Osteoarthritis, the degenerative inflammatory bone disease, may be a sign of faster "biological ageing," suggests research published ahead of print in the Annals of the Rheumatic Diseases.

The authors base their findings on a study of almost 1100 people, aged between 30 and 79. Most of them were female twins.

X-rays of both hands were taken of all participants to check for signs of osteoarthritis and a blood sample was taken to assess "biological ageing" in white cell DNA.

Biological ageing is likely to be reflected by the gradual shortening of telomeres, the length of DNA which caps the tips of chromosomes. A host of factors make them shorten over time, including insufficient repair of the damage caused by oxygen free radicals (oxidative stress).

Oxygen free radicals are the unstable molecules produced as a by-product of normal bodily processes, as well as external factors, such as tobacco, alcohol, and sunlight.

Osteoarthritis is the most common form of arthritis, with the hands being one of the sites most often affected. Its frequency rises dramatically with age, but it is still not known exactly what causes it.

Unsurprisingly, the findings showed that white cell telomere lengths were associated with chronological age. The older a person was, the shorter they were.

But among the 160 people with hand osteoarthritis, the telomere length was significantly shorter than among those without the disease, even after taking account of influential factors, such as obesity, age, sex, and smoking.

All those with hand osteoarthritis were over 50, and the amount of telomere shortening was equivalent to that accrued over 11 years in healthy people (178 base pairs).

Telomere length was also significantly associated with the severity of osteoarthritis. The more severe the disease, the shorter was the telomere length.

The authors suggest that both the ageing process and osteoarthritis share biological factors in common, including oxidative stress and low level chronic inflammation.
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PostPosted: Tue Oct 03, 2006 12:38 pm    Post subject: A Woman's Skin Ages Faster Reply with quote

A Woman's Skin Ages Faster

By Sara Goudarzi
LiveScience Staff Writer
posted: 03 October 2006
12:06 pm ET

Men become more distinguished as they age and women, well, we just keep getting older. And if this isn't bad enough, a new study shows that the female skin actually starts to age faster than the hides of men.

Using a new laser imaging technique, researchers looked at the deeper layers of the skin and measure the amount of damage from sun exposure and aging. The imaging of collagen and elastin, whose degeneration causes wrinkles and loss of smoothness, revealed that women lose collagen faster than men.

For the full article:

http://www.livescience.com/hum....._skin.html
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PostPosted: Mon Oct 09, 2006 9:33 am    Post subject: Everybody dance: The energy you use won't shorten your life Reply with quote

American Physiological Society
9 October 2006

Everybody dance: The energy you use won't shorten your life

VIRGINIA BEACH, VA (October 9, 2006) – The theory that animals die when they've expended their lifetime allotment of energy may be reaching the end of its own life, according to a study presented at The American Physiological Society conference, Comparative Physiology 2006. However, the longitudinal study leaves open a newer form of the theory -- that antioxidants help prolong life by limiting the damage that oxidative stress can cause to cells.

"These findings join a growing body of evidence suggesting that lifetime energy expenditure per se does not underlie senescence," wrote Lobke Vaanholt, Serge Daan, Theodore Garland Jr. and G. Henk Visser in a summary of the study presented at Comparative Physiology 2006: Integrating Diversity. Vaanholt, Daan and Visser are from the University of Groningen, The Netherlands. Garland is from the University of California at Riverside. The conference takes place Oct. 8-11 in Virginia Beach, Virginia.

A bit of background: One early theory, the rate of living theory, held that every organism has a set amount of energy to expend. Once the animal expended that number of calories, the grim reaper was on the doorstep. Over the years, the theory has become much more sophisticated, but metabolic rate and aging have remained linked, Vaanholt explained.

Decades ago, physiologists discovered that during metabolism, oxygen (O2) can split into single oxygen atoms, known as free radicals. These rogue oxygen atoms can remain on their own or combine with hydrogen atoms to form reactive oxygen species (ROS), which wreak havoc with enzymes and proteins and adversely affect cell function. The faster the metabolism, the more ROS produced, the modern theory goes.

Energy expenditure not the key

In this study the researchers divided the mice into three groups of 100 mice each. Two groups were "runner" mice, that is, mice that loved to run on the running wheels placed in their cages. One group of runner mice had access to running wheels, but the second group of runner mice did not. The third group consisted of regular laboratory mice that had a running wheel.

Vaanholt's team followed 60 mice from each of the three groups throughout their natural lives, nearly three years. They measured wheel running activity and took periodic measurements of body mass.

They found:


Runner mice that had access to a wheel expended 25% more energy over the course of their lives compared to both the runner group that did not have a wheel and the regular mice

Both groups of mice bred for running, one group with the wheel and one without, lived about 90 days less than the regular mice

The regular (non-runner) mice lived longest, 826 days, compared to the runners with a wheel, 735 days and runners without a wheel, 725 days

The rate of living theory would have predicted that the running group that expended more energy would die earlier than the two groups that did not, Vaanholt said. This was not the case. There was no difference in life span between the two runner groups, even though one expended more energy.

In addition, the rate of living theory would have predicted that the runner mice without the wheel and the normal mice would live approximately the same life span because there was no difference in energy expenditure between the two. This was not the case. The runner mice without the wheel died sooner.

"The shorter life span cannot, therefore, be explained by a difference in metabolism," Vaanholt concluded. "There must be something else going on that causes these animals to age and die."

More activity = higher metabolism = more antioxidants?

A second portion of the experiment involved the remaining 40 mice in each of the three groups. The researchers periodically used mice from these three groups to determine energy expenditure, body composition and the antioxidant enzyme levels and protein synthesis in the heart and liver tissues. The researchers selected mice, at two months, 10 months, 18 months and 26 months for this analysis.

Since the group of runner mice that expended more energy lived as long as the runner group that was less active, the researchers tested whether there was a difference in antioxidant production between the two groups. Since metabolic rate rises with activity level and oxidative stress rises with metabolic rate, perhaps the runner mice that expended more energy also produced more antioxidants, the body's defense against oxidative stress, Vaanholt said.

However, the study found no difference in antioxidant levels among the groups, at least in the heart and the liver, regardless of energy expenditure. "We would have expected additional antioxidants among the group of mice that expended 25% more energy, but that was not the case," Vaanholt said.

"We can conclude that the presence of a running wheel resulted in increased daily energy expenditure without a change in lifespan or in antioxidant enzyme activity in the heart and liver," Vaanholt explained.

Further research must examine whether tissues in other areas of the body generated additional antioxidants to help cope with the increased oxidative stress brought on with increased activity and metabolic rate, she said. In addition, future studies may examine whether other mechanisms are at work, including whether activity level is connected to DNA repair rates.


###
The American Physiological Society was founded in 1887 to foster basic and applied bioscience. The Bethesda, Maryland-based society has 10,500 members and publishes 14 peer-reviewed journals containing almost 4,000 articles annually.

APS provides a wide range of research, educational and career support and programming to further the contributions of physiology to understanding the mechanisms of diseased and healthy states. In 2004, APS received the Presidential Award for Excellence in Science, Mathematics and Engineering Mentoring.
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PostPosted: Sat Mar 10, 2007 8:18 am    Post subject: When your brain talks, your muscles don’t always listen Reply with quote

When your brain talks, your muscles don’t always listen
University of Delaware

8:43 a.m., March 9, 2007--Have your neurons been shouting at your muscles again? It happens, you know.

As we grow older, neurons--the nerve cells that deliver commands from our brains--have to “speak” more loudly to get the attention of our muscles to move, according to University of Delaware researcher Christopher Knight, an assistant professor in UD's College of Health Sciences.

For the full article:

http://www.udel.edu/PR/UDaily/.....30907.html
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PostPosted: Wed Mar 14, 2007 7:15 am    Post subject: Aging boosts chances that a family line will be long-lived Reply with quote

University of Washington
13 March 2007

Aging boosts chances that a family line will be long-lived

It is an inevitability of life – you are born and you begin to age.

Scientists have puzzled over just why organisms evolved aging as a strategy, and now there appears to be an answer. Allowing one individual to carry all the cellular damage inflicted over time, rather than dividing it between two organisms during reproduction, increases the chances that the individual's line will continue to reproduce for many generations to come, a new study indicates.

The earliest organisms, single-celled creatures called prokaryotes, which include bacteria, probably did not age but rather divided damaged material equally among new cells. There was not a parent cell, but rather the original cell divided into two siblings that were, in effect, the same age and shared the damage from the original cell equally.

Somewhere along the way, that strategy changed so that a parent cell retained most of the damage from aging and the offspring started with a mostly clean slate.

"The idea is that the damage has a constant effect on the fitness of the offspring, but if the damage is concentrated in one individual then a lot of damage will be eliminated from the lineage when that individual dies," said Carl Bergstrom, a University of Washington associate professor of biology who participated in the work.

Aging is essentially a decline in reproductive rate and an increase in mortality over time, based on changes in tissues, cells and cellular structures. Those changes can include damage to DNA or damage to cellular material or even organs.

In what is called symmetric reproduction, a cell divides in two and splits the damage equally among the succeeding generation of cells. In asymmetric reproduction, the parent retains the damage associated with aging.

Symmetric reproduction favors a longer life for an individual, but eventually the damage is likely to be so great that a particular line will no longer be able to reproduce. Asymmetric reproduction likely means a shorter life for an individual in exchange for the likely greater longevity of the line.

"If you divide asymmetrically, the survivor is likely to be the undamaged one, which will then be in a better position to produce surviving offspring," Bergstrom said.

The mechanisms that favor asymmetrical aging over symmetry are so general that they are expected to operate in a wide range of organisms, the researchers say. The new work suggests that aging has evolved in most – perhaps even all – types of organisms.

The research is described in a paper in the April edition of the journal Aging Cell. The lead author is Martin Ackermann of the Institute for Integrative Biology in Zurich, Switzerland. Besides Bergstrom, co-authors are Lin Chao of the University of California, San Diego, and Michael Doebeli of the University of British Columbia in Vancouver.

The researchers used mathematical models and computer simulations to examine the likely evolution of aging by distributing damage asymmetrically during reproduction. They also studied the investment an organism makes in a mechanism to repair damage. From their findings, the scientists concluded that reproduction in which damage was distributed asymmetrically would be favored.

The models were altered to allow cells to repair some of their damage, and asymmetric reproduction still was favored. Not only that, but once asymmetric division became the dominant reproduction method the models indicate that evolution will eventually reduce the investment in repair, Bergstrom said.

The implication is that evolution favors individuals aging as a means of allowing their lineage to persist longer.

"A lineage is more likely to survive in the long run if one individual falls on the grenade of its own cellular damage," Bergstrom said.

###
The work was funded by the Swiss National Science Foundation, the Roche Research Foundation, the Novartis Foundation, the U.S. National Institutes of Health, the James S. McDonnell Foundation and the Natural Sciences and Engineering Research Council of Canada.
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PostPosted: Wed Mar 21, 2007 7:06 am    Post subject: Aging Muscles Become Hard of Hearing Reply with quote

Aging Muscles Become Hard of Hearing

By Sara Goudarzi
LiveScience Staff Writer
posted: 20 March 2007
01:34 pm ET

As people age, neurons have to yell louder at the body's muscles to whip them into action, according to a new study, but exercise could reverse the aging effect.

Researchers examined the relationship between neuron activity and corresponding muscle force for 23 subjects between the ages of 18 and 88. They found a diminished ability of the muscles to respond to the commands of neurons amongst the older participants.

Specifically, the researchers looked at the dorsal interosseous muscle, situated between the index finger and thumb. This muscle is activated by 120 individual neurons. Each subject had a small needle-like electrode inserted into their index finger. The electrode was hooked up to a computer which recorded the electrical impulses as they traveled from the neurons to the muscle fibers.

For the full article:

http://www.livescience.com/hum.....s_age.html
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PostPosted: Mon Apr 02, 2007 8:29 am    Post subject: It's never too late to get it back! Aging interrupted Reply with quote

Society for Experimental Biology
1 April 2007

It's never too late to get it back! Aging interrupted

Much research has shown that reduced calorie intake can increase health and longevity. Professor Stephen Spindler (University of California) and his collaborators* have discovered that reducing calorie intake later in life can still induce many of the health and longevity benefits of life-long calorie reduction. Importantly, this also includes anti-cancer effects. They are using this knowledge to establish a novel screening technique to find drugs which mimic this longevity effect. “Right now, there are no authentic “anti-ageing drugs” capable of extending the lifespan of healthy people. The technique we have developed allows us to screen a relatively large number of drugs in months rather than years. The hope is that these drugs will be able to extend the lifespan of healthy animals, and possibly, after further testing, healthy humans”, says Professor Spindler who will present his results at the Society for Experimental Biology’s Main Meeting in Glasgow on Monday 2nd April.

Previous research has show that mice can live up to 40% longer if they simply consume fewer calories, but a highly nutritious diet. Because people are not very good at dieting, Dr. Spindler and his colleagues would like to identify drugs which can produce the same beneficial health and longevity effects without the low calorie diet. The problem is to find a way to rapidly identify these drugs. Professor Spindler and his colleagues are examining the gene expression patterns which are induced by low calorie diets, and looking for drugs which mimic these changes. They are searching for drugs which will have these beneficial effects and slow ageing, even when they are given late in life. One drug, normally used to treat diabetic patients, seems to produce many of the beneficial effects of a low calorie diet. However, it is important to be sure that healthy people will benefit from the drug. A very low level of toxicity could interfere with the beneficial effects of such a drug, if it is taken for a lifetime.

Physiological changes associated with ageing include cell damage and the emergence of cancer cells. The most important effects of low calorie diets and longevity therapeutics given late in life may not be to prevent this damage, but instead to stimulate the body to eliminate damaged cells that may become cancerous, and to stimulate repair in damaged cells like neurons and heart cells. Low calorie diets drive the body to replace and repair damaged cells. This process usually slows down as we age, but low calorie diets make the body re-synthesise and turn over more cells – a situation associated with youth and good health. Dr. Spindler and his colleagues used their screening method to search for drugs which cause pre-cancerous and cancerous cells to commit suicide and to replace those cells with new, healthy cells. It is thought that the body does this because it normally kills some cells like damaged and rogue cancer cells to provide energy when it is starving. Then it replaces these cells when a meal is eaten.

It seems it is the total number of calories which are consumed, rather than the type of food which is the key to the effects of low calorie diets on the ageing process. However, it is known that vegetarians and fish eaters live longer than red meat eaters, and that, generally, the more fruit and vegetables in the diet, the better your health and longer your lifespan.

###
*This work is a collaboration between Professor Spindler and Dr Joseph Dhahbi (Children’s Hospital Oakland Research Institute).

Published review paper (in press): S. Spindler and J. Dhahbi. 2007. Conserved and tissue-specific genic and physiologic responses to caloric reduction and altered IGF1 signalling in mitotic and post-mitotic tissues. Annual Review of Nutrition, 2007.
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PostPosted: Tue Apr 24, 2007 9:10 am    Post subject: Corn, oats, cherries and red wine’s high melatonin content c Reply with quote

Corn, oats, cherries and red wine’s high melatonin content can help delay ageing
University of Granada
24 April 2007

- A study carried out by researchers from the University of Granada’s Institute of Biotechnology proves that consuming melatonin neutralizes oxidative damage and delays the neurodegenerative process of ageing.
- In this study researchers used normal and genetically-modified mice which were subjected to accelerated cell ageing, although their results can also be applied to humans.


C@MPUS DIGITAL The Spanish Ageing Research Network (Red Nacional de Investigación del Envejecimiento), funded by Carlos III Health Institute and headed by professor Darío Acuña Castroviejo, from the University of Granada (Universidad de Granada), is very near to achieving one of today’s Science greatest goals: allowing humans to age in the best possible health conditions.

As well as from the UGR, researchers from the Spanish universities of Seville, Oviedo, Saragossa, Barcelona and Reus also took part in this study, concluding that the consumption of melatonin – a natural substance produced in small amounts by human beings and present in many types of food – delays the oxidative damage and inflammatory processes typical of the old age. Melatonin can be found in small amounts in some fruits and vegetables, like onions, cherries and bananas, and in cereals like corn, oats and rice, as well as in some aromatic plants, such as mint, lemon verbena, sage or thyme, and in red wine.

UGR participation in this study was leaded by professor Darío Acuña Castroviejo, member of the Institute of Biotechnology and lecturer at this University’s department of Physiology. Professor Acuña Castroviejo also coordinates the Spanish Ageing Research Network. Both normal and genetically-modified mice, with an accelerated cell ageing, were analysed. "We proved", says professor Acuña Castroviejo, “that the first signs of ageing in animal tissues start at the age of five months [in mice] – equivalent to 30 human years of age – due to an increase in free radicals (oxygen and nitrogen), which cause an inflammatory reaction.”

The UGR researcher points out that such oxidative stress also has effects in animals’ blood, as blood cells have been proven to be “more fragile with the years and, therefore, their cell membranes become easier to break".

Use in mice

The authors of this innovative finding administered small amounts of melatonin to mice and observed that not only did this substance neutralize the oxidative stress and the inflammatory process caused by ageing, but it also delayed its effects, thus increasing longevity. In particular, the University of Granada’s goal was to analyse the mitochondrial function in mice and check their mitochondrial capacity to produce ATP – adenosine triphosphate – a molecule whose mission is to store the energy every cell needs to carry out its functions.

Professor Acuña Castroviejo highlights that chronic administration of melatonin in animals from the moment they stop producing this substance – five months of age in mice – helps counteract all age-related processes. Therefore, daily melatonin intake in humans from the age of 30 or 40 could prevent – or, at least, delay – illnesses related to ageing, free radicals and inflammatory processes, such as many neurodegenerative disorders (e.g. Parkinson's disease) and complications linked to other illnesses, like diabetes.

The researcher is confident that the Spanish Ministry of Health will soon legalise the use of melatonin since, being a substance naturally produced by the body, it cannot be patented and the drug industry would not make much profit out of its artificial production. However, “while the substance becomes legalised, humans should try to increase melatonin consumption through food", recommends professor Acuña Castroviejo.

The results of this study have been published in some of the world’s most prestigious medical journals, such as Free Radical Research, Experimental Gerontology, Journal of Pineal Research and Frontiers in Bioscience.

Reference: Prof. Darío Acuña Castroviejo. Institute of Biotechnology, University of Granada.
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PostPosted: Mon Apr 30, 2007 9:31 am    Post subject: Study Suggests Why Elderly are Good Scam Targets Reply with quote

Study Suggests Why Elderly are Good Scam Targets

By Jeanna Bryner
LiveScience Staff Writer
posted: 30 April 2007
12:57 pm ET

The possibility of losing money stresses young adults out, but it doesn’t seem to faze the elderly.

New research reveals that while both young and old adults had similar levels of brain activity when anticipating rewards, certain brain regions in older adults didn’t activate when responding to a potential financial loss.

Published in the April 29 online edition of the journal Nature Neuroscience, the results add to the understanding of how age affects mental processes. It could also explain why older people are more susceptible to monetary scams.

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http://www.livescience.com/hum.....rains.html
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PostPosted: Thu May 17, 2007 12:44 pm    Post subject: Lipoic acid explored as anti-aging compound Reply with quote

Oregon State University
17 May 2006

Lipoic acid explored as anti-aging compound

PORTLAND, Ore. – Researchers said today they have identified the mechanism of action of lipoic acid, a remarkable compound that in animal experiments appears to slow down the process of aging, improve blood flow, enhance immune function and perform many other functions.

The findings, discussed at the "Diet and Optimum Health" conference sponsored by the Linus Pauling Institute at Oregon State University, shed light on how this micronutrient might perform such a wide range of beneficial functions.

"The evidence suggests that lipoic acid is actually a low-level stressor that turns on the basic cellular defenses of the body, including some of those that naturally decline with age," said Tory Hagen, an LPI researcher and associate professor of biochemistry and biophysics at OSU. "In particular, it tends to restore levels of glutathione, a protective antioxidant and detoxification compound, to those of a young animal. It also acts as a strong anti-inflammatory agent, which is relevant to many degenerative diseases."

Researchers at LPI are studying vitamins, dietary approaches and micronutrients that may be implicated in the aging or degenerative disease process, and say that lipoic acid appears to be one of those with the most compelling promise. It's normally found at low levels in green leafy vegetables, but can also be taken as a supplement.

According to Hagen, research on the natural processes of aging, and steps that could slow it or improve health until near the end of life, are of growing importance.

"We're coming into the middle of an aging epidemic in the country," he said. "In a short time more than 70 million Americans will be over 65. This is partly because of the Baby Boom, but also people are living longer, being saved with antibiotics and other medical treatments. In any case, it will be an unprecedented number of elderly people in this nation."

The goal of LPI research, Hagen said, is to address issues of "healthspan," not just lifespan – meaning the ability to live a long life with comparatively good health and vigor, free of degenerative disease, until very near death. The best mechanisms to accomplish that, scientists say, have everything to do with diet, exercise, healthy lifestyle habits and micronutrient intake.

At the moment, Hagen said, that's not the way things appear to be headed – diabetes is skyrocketing, about 50 percent of people over 65 have high blood pressure, heart disease often leads to permanent disability, and almost half of the elderly people in America have malnutrition that is easily preventable.

No single intervention can address all of these issues, Hagen said, but one that scientists keep coming back to is lipoic acid.

"Our studies have shown that mice supplemented with lipoic acid have a cognitive ability, behavior, and genetic expression of almost 100 detoxification and antioxidant genes that are comparable to that of young animals," Hagen said. "They aren't just living longer, they are living better – and that's the goal we're after."

What the OSU researchers now believe is that the role of lipoic acid is not so much a direct one to benefit cells, but rather an indirect aid that "kick starts" declining function in cells and helps them recover the functions that came more easily and naturally in young animals.

In various effects, lipoic acid appears to help restore a cellular "signaling" process that tends to break down in older blood vessels. It reduces mitochondrial decay in cells, which is closely linked to the symptoms of aging. With age, glutathione levels naturally decline, making older animals more susceptible to both free radicals and other environmental toxins – but lipoic acid can restore glutathione function to near normal. And the expression and function of other genes seems to come back to life.

"We never really expected such a surprising range of benefits from one compound," Hagen said. "This is really unprecedented, and we're pretty excited about it."

Many other presentations have been made at this conference on the role of diet, lifestyle and micronutrients in health and degenerative disease, including cancer, heart disease, neurological diseases and aging.

The conference is organized every two years by OSU's Linus Pauling Institute, and attracts leading experts from around the world in these research fields.
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PostPosted: Mon May 21, 2007 8:31 pm    Post subject: Retinol lotion reduces the fine wrinkles from natural aging Reply with quote

University of Michigan Health System
21 May 2007

Retinol lotion reduces the fine wrinkles from natural aging of skin

Products previously were thought only to improve skin aged by sun
ANN ARBOR, Mich. — Lotions containing retinol improve the appearance of skin that has become wrinkled through the normal aging process, not just skin that has been damaged by exposure to the sun, according to a new study from the University of Michigan Health System.

Researchers tested lotions containing retinol – Vitamin A that is found in many skin-care products – on the skin of elderly patients. Lotion containing retinol was used on one arm of each participant, while a lotion without retinol was applied to the other arm.

Wrinkles, roughness and overall aging severity were all significantly reduced in the retinol-treated arm compared with the control arm, according to the study, which appears in the May issue of the journal Archives of Dermatology. The production of collagen, due to the retinol treatment, also makes it more likely that the skin can withstand injury and ulcer formation, researchers say.

“With the population aging so rapidly, it is important that we find ways of treating skin conditions of elderly people – not just for purposes of vanity, but also for the healing of wounds and the reduction of ulcers,” says senior author Sewon Kang, M.D., professor of dermatology at the U-M Medical School.

This research serves as an important step forward in the understanding of how aging skin can be improved, researchers say.

“In the past, it was everyone believed that retinoids would treat only photoaging, or damage from exposure to sun. This is the first systematic, double-blind study showing that it improves any kind of aging – photoaging as well as natural aging,” says co-author John J. Voorhees, M.D., the Duncan and Ella Poth Distinguished Professor and chair of the Department of Dermatology at the U-M Medical School. “You can rub it anywhere, and it will help to treat the signs of aging.”

The lotion was made at U-M, but U-M will not commercialize this lotion because it was designed only for experimental purposes and, therefore, is cosmetically undesirable. Many retinol containing cosmeceutical creams, however, are sold by various companies. Those specific products were not tested by the U-M team.

The reduction of wrinkles in the study’s participants was due to increased collagen production and a significant induction of glycosaminoglycans, which are known to retain large quantities of water. In general, aging skin tends to be thinner, laxer and more prone to fine wrinkles than young skin.


###
In addition to Kang and Voorhees, authors of the study were lead author Reza Kafi, M.D.; Heh Shin Kwak, M.D.; Wendy E. Schumacher, B.S.; Soyun Cho, M.D., Ph.D.; Valerie N. Hanft, M.D.; Ted A. Hamilton, M.S.; Anya L. King, M.S.; Jacqueline D. Neal, B.S.E.; James Varani, Ph.D.; and Gary J. Fisher, Ph.D. All of the authors were at the University of Michigan Department of Dermatology when they participated in the study. Kafi and Kwak now are at Stanford Medical School, and Cho is with the Seoul National University in South Korea.

Fisher, Kang, Varani and Voorhees are named inventors on an issued patent application concerning methods for treating skin aging. They would receive royalties under U-M’s Intellectual Property Policy in the event that a commercial license is signed and a product is sold. This article describes research that was part of the basis of the approved application.

The study was supported in part by grants from the Babcock Endowment for Dermatologic Research, the Merck-American Federation for Aging Research, Alpha Omega Alpha Student Research Fellowship and the National Institutes of Health.

Reference: Archives of Dermatology, May 2007, Vol. 143: 606-612.
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PostPosted: Tue May 22, 2007 9:45 am    Post subject: Men's Minds Decline More with Age Reply with quote

Men's Minds Decline More with Age
By Andrea Thompson, LiveScience Staff Writer

posted: 21 May 2007 08:13 am ET

Everyone becomes a little more forgetful as they get older, but men's minds decline more than women's, according to the results of a worldwide survey.

Certain differences seem to be inherent in male and female brains: Men are better at maintaining and manipulating mental images (useful in mathematical reasoning and spatial skills), while women tend to excel at retrieving information from their brain's files (helpful with language skills and remembering the locations of objects).

Many studies have looked for a connection between gender and the amount of mental decline people experience as they age, but the results have been mixed.

For the full article:

http://www.livescience.com/hea.....minds.html
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PostPosted: Sat Jun 02, 2007 7:58 am    Post subject: Agent slows aging in mice Reply with quote

University of Michigan Health System
1 June 2007

Agent slows aging in mice

Compound derived from creosote bush shows early potential
ANN ARBOR, Mich. -- Aspirin didn’t pan out. Neither did two other potential anti-aging agents. But a synthetic derivative of a pungent desert shrub is now a front- runner in ongoing animal experiments to find out if certain chemicals, known to inhibit inflammation, cancer and other destructive processes, can boost the odds of living longer.

Today at the annual meeting of the American Aging Association, University of Michigan scientist Richard A. Miller reports early results from a mouse study his lab and two others are conducting for the National Institute on Aging. The study, now in its fourth year, will test as many as two dozen possible anti-aging agents in animals in the next five years. The other centers are the University of Texas Health Science Center in San Antonio, Texas, and the Jackson Laboratory in Bar Harbor, Maine.

The scientists were surprised to find so quickly that one agent showed promise: NDGA, a compound derived from creosote bushes. These common North American desert shrubs have been traditionally used by Native Americans as healing remedies.

The preliminary results, to be published in August in the journal Aging Cell, show that male mice fed a normal diet and NDGA so far have survived in significantly greater numbers than mice on a normal diet. Scientists measured the difference at a point called median lifespan, when half the control mice had died of natural causes associated with aging.

“This is the first time to my knowledge when an agent has been shown to extend median life span in three laboratories,” says Miller, professor of pathology at the U-M Medical School and associate director of the U-M Geriatrics Center. Miller is also a research scientist at the Ann Arbor VA Medical Center.

No significant difference occurred in female mice. The scientists can’t explain why at this point. “We don’t know how NDGA is having its effect on survival in this first analysis,” Miller says.

“It may be that the female mice because of their hormonal status have other pathways to death and disability, or need higher or lower levels of NDGA to see an effect.”

The large, carefully controlled study at three sites, called the NIA Interventions Testing Program, is intended to provide some of the first reliable data on potential drugs to slow aging and its accompanying ills.

Miller says prior studies typically have been too small and their results hard to confirm in subsequent studies. “The National Institute on Aging decided to fund grants at three institutions to do studies of this sort in the right way,” he says.

In six to 10 months, once all the mice in the control group have died, the scientists will get answers to the really burning question: Will the mice fed NDGA, already well past middle age, live past the normal outer limit of old age" The longest that mice of this type usually live is around 1,000 to 1,100 days.

“If NDGA turns out to extend maximal lifespan by 20 or 30 percent, people would accept that as an important finding,” Miller says.

No one excited by these early results in mice is advised to bulk up on creosote bush leaves as a way to defy old age. If NDGA pushes the aging envelope in the final results of this study, other labs will likely try to repeat the results in animals. Much more research is needed before any possible human anti-aging drug could emerge, Miller says.

“Even if this agent turns out to be good for mice, it won’t be possible to tell without careful studies of humans whether NDGA is beneficial, useless, or harmful to people. Occasionally, something that is harmless in mice turns out to be highly toxic for people,” Miller cautions, adding that the Food and Drug Administration doesn’t evaluate the safety of such herbal remedies.

###
Randy Strong of the University of Texas Health Science Center, David E. Harrison of the Jackson Laboratory and Miller are chief collaborators in the National Institute on Aging project, which includes scientists at Oklahoma Medical Research Foundation, the University of Florida, and Milan, Italy.

The research is funded by the National Institute on Aging, part of the National Institutes of Health.

Visit www.americanaging.org for more information on the American Aging Association and its annual meeting.
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PostPosted: Wed Jun 06, 2007 2:04 pm    Post subject: Aging stem cells in mice may hold answers to diseases of the Reply with quote

Stanford University Medical Center
6 June 2007

Aging stem cells in mice may hold answers to diseases of the aged, Stanford study finds

STANFORD, Calif. -- As stem cells in the blood grow older, genetic mutations accumulate that could be at the root of blood diseases that strike people as they age, according to work done in mice by researchers at the Stanford University School of Medicine.

"This and our previous work points out why older people are more likely to get blood diseases, such as leukemia or anemia, and are less likely to make new antibodies that would protect against infections like the flu," said senior author Irving Weissman, MD, director of the Stanford Institute for Stem Cell Biology and Regenerative Medicine and of the Stanford Comprehensive Cancer Center. The work will be published in the June 6 issue of Nature.

In past studies, this group of researchers had shown that blood-forming stem cells in the bone marrow of mice became less able to divide and replenish the supply of blood cells as they aged. The question was why.

Researchers have put forward many theories about how cells age, said Derrick Rossi, PhD, postdoctoral scholar and co-first author of the paper. One of those theories has to do with cells accumulating genetic mutations. "The idea is that, over time, accumulated DNA damage progressively diminishes the cell's ability to perform its normal function," he said.

However, researchers had thought that mutations were unlikely to underlie aging in blood-forming stem cells because they very rarely divide, and most mutations crop up during division. The infrequent divisions were believed to protect the cells from acquiring new mutations.

Rossi, Weissman and the other first author, postdoctoral scholar David Bryder, PhD, tested that idea in two different sets of experiments. In the first, they studied the blood-forming stem cells of mice engineered to have single mutations that make them especially prone to accumulating additional genetic errors. In each of the three different types of mutant mice they studied, the stem cells appeared to behave normally and to produce new blood cells.

However, the full truth came out when they took blood-forming stem cells from any of the three types of mice and used those cells to repopulate the bone marrow of irradiated mice. This type of experiment is much like using a bone marrow transplant to bring back the bone marrow in a person who has undergone extensive chemotherapy.

Normally, a few stem cells are enough to completely replenish the bone marrow of mice and produce normal amounts of blood and immune cells. However, error-filled blood-forming stem cells taken from the mutant mice were much less effective at colonizing the depleted bone marrow than normal stem cells, and became even less effective when taken from older mutant mice.

Rossi said these results suggest that mutations accumulating in stem cells as they age were preventing them from doing their normal job of producing new blood and immune system cells. However, these results were in mutant mice. Rossi wanted to know if the stem cells in normal, healthy mice also accumulate damage as they age.

To address this, in the second set of experiments, Rossi isolated stem cells from the bone marrow of normal young and old mice, then stained those cells with a chemical that clings to a protein that's associated with DNA damage. This protein can act as a flag to highlight nearby DNA damage.

What he found is that young stem cells from normal mice contained no stain and therefore little or no DNA damage. Older stem cells, on the other hand, showed extensive staining.

All of this adds up to one thing: blood-forming stem cells do accumulate DNA damage with age even though they rarely divide, and that damage is passed on to the blood and immune system cells they make. Weissman said these findings could explain the origin of blood cancer (leukemia) and immune dysfunctions that occur as people age.

The next step is to show whether these results from mice hold true for human blood-forming stem cells. "If this work does extrapolate to humans, then it is absolutely consistent with the idea that blood-forming stem cells are the breeding ground for pre-leukemic mutations," said Weissman, the Virginia and D.K. Ludwig Professor for Clinical Investigation in Cancer Research.
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PostPosted: Wed Jul 11, 2007 8:08 am    Post subject: No Joke: Age Makes Things Less Funny Reply with quote

No Joke: Age Makes Things Less Funny
By Betsy Taylor, Associated Press

posted: 10 July 2007 05:50 pm ET

ST. LOUIS (AP) -- A new psychology study at Washington University was no laughing matter: It found that older adults may have a harder time getting jokes because of an age-related decline in certain memory and reasoning abilities.

The research suggested that because older adults may have greater difficulty with cognitive flexibility, abstract reasoning and short-term memory, they also have greater difficulty with tests of humor comprehension.

Researchers tested about 40 healthy adults over age 65 and 40 undergraduate students with exercises in which they had to complete jokes and stories. Participants also had to choose the correct punch line for verbal jokes and select the funny ending to series of cartoon panels.

For the full article:

http://www.livescience.com/hea.....aging.html
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PostPosted: Mon Aug 06, 2007 12:00 pm    Post subject: Theory of facial aging gets a facelift from UT Southwestern Reply with quote

UT Southwestern Medical Center

Theory of facial aging gets a facelift from UT Southwestern researchers

DALLAS – Aug. 6, 2007 – The longstanding idea that the entire human face ages uniformly is in need of a facelift, say researchers at UT Southwestern Medical Center who have found that multiple, distinct compartments of fat in the face age at different rates.

The findings, published in a recent issue of Plastic and Reconstructive Surgery, challenge previously held theories regarding aging and may offer new ways to help turn back the clock, UT Southwestern plastic surgeons say.

“For hundreds of years, everyone has believed that the fat on the face is one confluent mass, which eventually gets weighed down by gravity, creating sagging skin,” said Dr. Joel Pessa, assistant professor of plastic surgery and the study’s lead author. “In our studies, however, we were surprised to find that this is not the case; the face is made up of individual fat compartments that gain and lose fat at different times and different rates as we age.”

The study involved injecting different types of dye into facial cavities of 30 cadavers. Despite at least 24 hours of settling time, the dye, rather than permeating the entire face, stayed in separate areas – showing that individual facial compartments have boundaries between them that act like fences. These fences, which seem to be composed of fibrous tissue, allow the face to maintain its blood supply should it become injured.

Dr. Pessa said the face resembles a three-dimensional puzzle, with fat divided into distinct units around the forehead, eyes, cheeks and mouth. Facial aging is, in part, characterized by how these separate compartments change as we grow older.

A youthful face is characterized by a smooth transition between these compartments. As people age, contour changes occur between these regions due to volume losses and gains as well as repositioning of the compartments. Eventually, this can result in sagging or hollowed skin and wrinkles.

“This is a revolutionary way of viewing facial anatomy. It not only tells us how we age, it shows us why we age the way we do, and why every part of the face, from the eyelids to the cheeks, ages differently,” said Dr. Rod Rohrich, chairman of plastic surgery and senior author of the study. “This will help plastic surgeons around the world not only understand how we can better rejuvenate the face, but how people age as a physiological process.”

This breakthrough could have tremendous implications in helping plastic surgeons target facial “trouble” areas and use injectible fillers to add volume to individual sections of the face. It could also aid in developing new and improved cosmetic and reconstructive surgery techniques, Dr. Rohrich said.

“Understanding how fat is compartmentalized will allow us to be very accurate and precise in how we approach facial rejuvenation,” Dr. Pessa said. “This gives us an algorithm, or scientific approach, to help ascertain what areas of the face may need extra fat to combat the aging process. It also is a major breakthrough in facial anatomy that will have major implications for future studies on aging and possibly hold clues to the study of other diseases such as obesity, diabetes and cancer.”


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This news release is available on our World Wide Web home page at

http://www.utsouthwestern.edu/home/news/index.html

http://www.utsouthwestern.edu/.....98396.html

To automatically receive news releases from UT Southwestern via e-mail, subscribe at www.utsouthwestern.edu/receivenews

Dr. Joel Pessa - http://www.utsouthwestern.edu/.....34,00.html

Dr. Rod Rohrich - http://www.utsouthwestern.edu/.....03,00.html
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PostPosted: Mon Oct 22, 2007 12:35 pm    Post subject: A longer-living, healthier mouse that could hold clues to hu Reply with quote

A longer-living, healthier mouse that could hold clues to human ageing
22 October 2007
University College London

A study by scientists at UCL (University College London) shows that mice lacking the insulin receptor substrate (IRS)-1 are more resistant to ageing than normal mice. The research adds to a growing body of work showing the importance of insulin signalling pathways as an ageing mechanism in mammals – and potentially humans.

The team studied ‘knock-out’ mice engineered to lack either insulin receptor substrate (IRS)-1 or -2. These proteins are activated by insulin, a hormone that regulates glucose and fat metabolism, informing the body’s cells when the animal is well fed.

The study, published in The FASEB Journal, shows that mice lacking IRS-1 had an average lifespan increase of 20 per cent when compared to normal mice. In female mice lacking IRS-1 this figure was even higher, averaging 30 per cent. While the expected life-span for a mouse is about 25 months, one of the IRS-1deficient mice in this research lived for 38 months – 66 per cent longer than a normal mouse.

As well as living longer, the mice without IRS-1 also experienced better health than the normal mice as they aged – they had brighter eyes, were more alert and were much healthier overall. In comparison, the mice that lacked IRS-2 were shorter-lived than the normal mice and displayed signs of obesity and type 2 diabetes.

Professor Dominic Withers, who works with the UCL Centre for Research on Ageing and is lead author of the study, said: “Our provisional results indicate that mice lacking IRS-1, particularly female mice, are more long-lived and show resistance to a range of markers that indicate ageing – including skin, bone, immune, and motor dysfunction.

“What’s more, these improvements were seen despite the fact that removing IRS-1 made the mice resistant to insulin throughout their lives. These results suggest that IRS-1 is a pathway conserved by evolution that regulates the lifespan of mammals, and it may point to methods of potentially delaying ageing in humans.

“We do not yet fully understand why lacking IRS-1 leads to longer life in mice. One possible explanation is that it makes them only mildly insulin resistant and that this, rather than having a negative effect on health, increases stress resistance, protects from damage and generally triggers other reactions in the body which extend life without compromising health.”

Dr David Gems, another of the study’s authors, added: “Other research has shown that mutations in single genes in the insulin pathway can extend the life of animals. However, our research adds new information because it shows that not only does manipulation of this pathway regulate how long animals live, it also shows that these effects allow the mice to stay healthier for longer. In these animals we see delay in the onset of age-related illnesses such as osteoporosis, diabetes and immune dysfunction. Obviously it’s much harder to study these mechanisms in humans because our life expectancy is so much longer, but this study and our other work on ageing are laying crucial scientific groundwork.”

The study follows other ageing research pioneered at the UCL Centre for Research on Ageing, led by Professor Linda Partridge. The teams at the Centre analyse the cellular and biochemical mechanisms of ageing in fruit flies, nematode worms and mice, and in particular the role of insulin signalling. Their work was recognised in June 2007 by a Strategic Award from the Wellcome Trust totalling £5.1 million, to support their work examining what causes human bodies to age and decay. The UCL Institute of Healthy Ageing, incorporating the existing Centre, will be established in 2008 and will encourage further collaboration between UCL scientists working in this area.
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PostPosted: Mon Oct 29, 2007 1:32 pm    Post subject: Visual field loss primary component in risk of falls for old Reply with quote

Association for Research in Vision and Ophthalmology
29 October 2007

Visual field loss primary component in risk of falls for older adults

Mobility training may help reduce fall risk
Rockville, MD þu Visual field loss (specifically peripheral visual fields) is the primary vision component that increases the risk of falls, according to a study published this month in Investigative Ophthalmology and Vision Science, a peer-reviewed monthly publication of the Association for Research in Vision and Ophthalmology (ARVO).

The authors of "Visual Field Loss Increases the Risk of Falls in Older Adults: The Salisbury Eye Evaluation" ( http://www.iovs.org/cgi/content/full/48/10/4445 ) ¡ª Ellen Freeman, Beatriz Munoz, Gary Rubin and Sheila West ¡ª looked at deficits in different components of vision to see if any were more closely linked with falls than others. The study primarily took place at Johns Hopkins School of Medicine¡¯s Wilmer Eye Institute in Baltimore, MD.

For each 10 percent loss in the visual field, people in the study experienced an 8 percent higher chance of falling after adjustment for other risk factors for falls. For example, persons with bilateral glaucoma, who on average would miss 48 points in the total visual field, would have 46 percent higher odds of falling.

The researchers used data from 2,375 people who participated in the Salisbury Eye Evaluation (SEE) over 20 months. SEE tested visual acuity, contrast sensitivity, visual field and stereoacuity at baseline. Participants recorded falls on a calendar that they sent to SEE each month.

The authors found that visual fields were associated with the risk of falling, while the other three components, after adjustments for demographics, were not. When they looked at the central and peripheral fields together, only the peripheral visual field was statistically significant.

Dr Freeman and her colleagues speculate that visual field reduction is most likely related to the risk of falls, at least in part, because of its affects on postural stability and aspects of mobility, which in turn is linked with the ability to maneuver around objects.

The authors conclude that people with visual field loss may benefit from mobility training to navigate the environment more safely and reduce the risk of falling.
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PostPosted: Mon Nov 05, 2007 5:32 pm    Post subject: Old Folks Focus Just Fine, Thanks Reply with quote

Old Folks Focus Just Fine, Thanks
By Andrea Thompson, LiveScience Staff Writer

posted: 04 November 2007 10:59 pm ET

Old folks can focus their attention on sights and sounds just as well as any young whippersnapper.

Previous research has indicated that elderly adults might be more distracted by sights or sounds that interfere with their focus, so a new study conducted by scientists at the Wake Forest University Baptist Medical Center set out to test whether this was really the case.

For the full article:

http://www.livescience.com/hea.....focus.html
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PostPosted: Tue Dec 04, 2007 3:01 pm    Post subject: Fighting diseases of aging by wasting energy Reply with quote

Cell Press
4 December 2007

Fighting diseases of aging by wasting energy

By making the skeletal muscles of mice use energy less efficiently, researchers report in the December issue of Cell Metabolism, a publication of Cell Press, that they have delayed the animals’ deaths and their development of age-related diseases, including vascular disease, obesity, and one form of cancer. Those health benefits, driven by an increased metabolic rate, appear to come without any direct influence on the aging process itself, according to the researchers.

The mitochondria powering the mouse muscles were made inefficient by increasing the activity of so-called uncoupling protein 1 (UCP1). UCP1 disrupts the transfer of electrons from food to oxygen, a process known as mitochondrial respiration, which normally yields the energy transport molecule ATP. Instead, the energy is lost as heat.

“When you make the mitochondria inefficient, the muscles burn more calories,” a metabolic increase that could be at least a partial substitute for exercise, said Clay Semenkovich of Washington University School of Medicine in St. Louis. “There are a couple of ways to treat obesity and related diseases,” he continued. “You can eat less, but that’s unpopular, or you could eat what you want as these animals did and introduce an altered physiology. It’s a fundamentally different way of addressing the problem.”

Atherosclerosis, diabetes, hypertension, and cancer occur more frequently with increasing age, the researchers explained. These age-related diseases are distinct from the process of aging, a physiological decline that includes decreases in muscle strength, cardiopulmonary function, vision, and hearing as well as wrinkled skin and graying hair. Thus, the researchers added, aging and age-related disease are associated but may not share the same mechanisms.

Given the difficulty of validating strategies to increase life span in humans and the possible dissociation between aging and age-related diseases, the researchers said, identifying a simple intervention affecting several age-related diseases is an attractive approach to decreasing the morbidity of growing old. They suspected that treatments designed to alter the efficiency of mitochondrial respiration might be one way to accomplish this.

Earlier studies had shown that young mice engineered to express modestly increased levels of UCP1 in skeletal muscle had a mildly increased metabolic rate, although they ate and grew normally. The animals’ muscles otherwise functioned as usual. In the new study, Semenkovich’s group used these mice to determine whether respiratory uncoupling in skeletal muscle—a tissue that adapts to altered heat production and oxygen consumption during exercise—can affect age-related disease.

They found that animals with increased UCP1 only in skeletal muscle lived longer. Altered female animals also developed lymphoma, a type of cancer that originates in white blood cells called lymphocytes, less frequently. In mice genetically predisposed to vascular disease, the increase in UCP1 led to a decline in atherosclerosis in animals fed a “western-type” high-fat diet. Likewise, mice predisposed to developing diabetes and hypertension were relieved of those ailments by increased UCP1 in skeletal muscle. The “uncoupled mice” also had less body fat (or adiposity) and higher body temperatures and metabolic rates, among other biochemical changes.

“The consequences of excess adiposity disproportionately affect older individuals,” the researchers concluded. “Excess adiposity can be treated through two simple approaches, decreasing energy intake or increasing energy consumption. Considerable effort is currently being devoted to the development of agents that decrease energy intake in hopes of decreasing adiposity and perhaps age-related disease. Our results indicate that increasing energy consumption in mice has beneficial effects on survival, vascular disease, elevated blood pressure, and diabetes. This intervention does not slow aging but may diminish susceptibility to pathology. Strategies to safely accelerate energy consumption specifically in skeletal muscle could decrease the impact of some common age-related diseases.”


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The researchers include Allison C. Gates, Carlos Bernal-Mizrachi, Sharon L. Chinault, Chu Feng, Jochen G. Schneider, Trey Coleman, James P. Malone, R. Reid Townsend, Manu V. Chakravarthy, and Clay F. Semenkovich, of the Washington University School of Medicine, St. Louis, MO, USA.
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