(HealthDay News) -- Canadian researchers have discovered a gene mutation that actually improves long-term memory and could eventually lead to a memory

(HealthDay News) -- What's the secret of those who survive into the triple-digits? It might be that they are keen on keeping up the latest trends, including iPods, current events and even MTV, a new survey finds.

In its second annual 100 at 100 Survey, Evercare, a health insurance plan that specializes in older people, polled 100 centenarians about their secrets of successful aging.
One of the respondents, George Reed, age 103, attributes his health and longevity to luck. But he has also spent much of his life being active, and remains so today.

Once an avid baseball player and cyclist, Reed still practices T'ai Chi daily, plays bingo and keeps up with news and current events.

"I read the newspaper rather regularly and manage to keep up with what's going on," Reed said.
The U.S. Census Bureau estimates that there are now more than 80,000 Americans 100 years of age or older. That number is expected to rise to more than 580,000 by 2040.

Among the main findings of the survey were the tendencies of centenarians to tune into trends and current events, lead healthy lifestyles and hold faith and spirituality in high regard, Dr. John Mach, CEO of Evercare, said in a prepared statement.

The survey found that nearly a third of the respondents have watched a reality TV show, and 27 percent have watched MTV or music videos.

Six percent have spent time on the Internet, and four percent said they have listened to music on an iPod.

When asked who they trust the most to tell the truth, 34 percent of the centenarians said they trusted their spiritual leader (e.g., priest, rabbi, minister). This echoed the results of last year's survey, which indicated the centenarians attribute their longevity to faith and spiritual care more than genes and medical care.

Reed, a practicing Catholic, agreed. "Prayer has gotten to be quite a thing with me," he said.
Eighty-two percent of the survey respondents said their dietary habits had improved or stayed the same, compared with 50 years ago.

While 40 percent of the respondents said they turn to newspapers for news and current events, 68 percent rely on television.

So, what do experts call the keys to successful aging?

While good genes can help you live a longer, healthier life, balancing your genes with a healthy lifestyle is also important, doctors say.

"Maintaining good health behaviors throughout one's life may lead to longer survival and better health," said Dr. Dellara Terry, co-director of the New England Centenarian Study and assistant professor at the Boston University School of Medicine.

Terry lists avoiding smoking, exercising regularly and eating a balanced diet (with reasonable portions) among health behaviors to aim for. She also advocates exercising your mind.
"In the context of 'use it or lose it,' " Terry said, "there is an increasing body of evidence that suggests exercising one's brain may in fact benefit one's health."

Terry and her colleagues are currently following more than 1,000 centenarians to see how genetic and environmental factors contribute to their health and longevity.

While you cannot have complete control over how long you will live, having good health habits, following your health care providers' advice and staying socially and mentally engaged will go a long way in improving the quality and -- perhaps -- the quantity of your life, the experts said.

More information
The Centers for Disease Control and Prevention has more about healthy aging.

Genetic Mutation Boosts Memory

(HealthDay News) -- Canadian researchers have discovered a gene mutation that actually improves long-term memory and could eventually lead to a memory-enhancing pill.

Working with mice, lead researcher Mauro Costa-Mattioli, a postgraduate fellow at McGill University in Montreal, and colleagues found that rodents that had a defective version of a gene that produces a memory-blocking protein could learn and remember tasks faster than normal mice.

"We discovered a protein that is called eIF2a that, when mutated, mice have an enhanced memory," Mattioli said. "We hope that this could be a good target to develop a compound that will mimic this mutation, and we can enhance memory in humans," he said.

In one experiment, the mice were trained to swim to a hidden platform. After several days of training, the mice with the gene mutation were able to find the platform significantly faster than normal mice, Mattioli said.

Mattioli likened it to reading pages of a textbook -- for most people, it might take several times to memorize everything. "But if a human had the same mutation, one would be able to remember it after one reading," he said.

To confirm that this gene mutation actually improved memory, the researchers treated the mutant mice with a molecule that increased the concentration of the memory blocker. When concentration of the memory-blocker was increased, the mice showed signs of memory impairment, Mattioli said.

The findings are published in the April 6 issue of the journal Cell.
Mattioli thinks that finding a way to get the same memory-enhancing effect in humans could benefit patients with memory loss, including Alzheimer's patients. "We wouldn't cure Alzheimer's, but, hopefully, we can rescue the memory deficit, which is associated with the disease," he said.

One expert thinks this discovery could be important in understanding memory loss in Alzheimer's disease.

"Many researchers are pursuing the hypothesis that memory loss in Alzheimer's disease is caused by defects in the complicated machinery controlling the formation of synapses -- the critical connections between nerve cells that define functional circuits," said Greg M. Cole, associate director of the UCLA Alzheimer's Disease Research Center, and a professor of medicine and neurology at the University of California, Los Angeles.

"The authors have added a fresh insight into one of the pathways that make new proteins for forming new long-term memories." Cole said. "How this pathway relates to diseases like Alzheimer's with loss of synapses and memory remains to be seen, but it is easy to guess that it could."

More information
To learn more about memory loss, visit the U.S. National Institute on Aging.

Dogged Research Spots Gene Behind Pooches' Size

(HealthDay News) -- Variation in just one gene turns a toy poodle into a standard and helps separate tiny Chihuahuas from massive Great Danes, new research shows.

"It's a gene called IGF1, for 'insulin growth factor 1'. We found a particular signature or pattern of variation for that gene in all small dogs, and we see a different pattern of variation in that gene when we look at the large breeds -- the St. Bernards and the Great Danes and Newfoundlands," said the study's senior researcher, Elaine Ostrander, chief of the cancer genetics branch at the U.S. National Human Genome Research Institute.

While dog lovers may be most interested in how the gene determines their pet's size, scientists like Ostrander say the discovery has much broader implications.

"Understanding the genetics of growth and regulation is key to understanding many disease processes that we see in both animals and humans, whether that's cancer, diseases of skeletal growth, hip dysplasia -- any of those things where cell division has gone awry," she said.

Other dog -- and medical -- experts agreed. "We're very excited about these findings, both with regard to the canine community and the implications for human research as well," said A. Duane Butherus, grants chairman of the American Kennel Club's Canine Health Foundation.

"The compact breeding cycles and well-documented pedigrees of purebred dogs are helpful tools in the search for genetic markers," he said. "The markers we find in canine research are often the candidate genes for human research as well, so 'man's best friend' is truly becoming man's best friend in the fight against disease," Butherus said.

The findings, based on a collaboration involving the National Human Genome Research Institute and a number of academic centers, are published in the April 6 issue of the journal Science.
According to Ostrander, dogs are ideal subjects for research into the genetics of cell growth. "Dogs differ in body mass by about 40-fold, and nowhere else among the land mammals do we see that amazing diversity and variation," she said.

Most of that variation is man-made, she added. As humans moved to a more settled, agrarian society more than 15,000 years age, they began domesticating young wolves to help protect them and to help them herd and hunt. That meant rapid specialization of canines.

"We strongly selected different breeds of dogs to have different features that would suit our lifestyle," Ostrander said. That produced everything from large, fleet-footed dogs (to help bring down game) to much smaller "ratters" for digging out ground-dwelling mammals, she said.
But why selectively breed dogs and not cats or pigs? According to Ostrander, Canis familiaris may have a distinct genetic advantage over other species.

Although it hasn't been proven yet, many scientists believe that "there is some kind of 'fast-forward' evolutionary mechanism in dogs that constantly throws up new (gene) variants much more quickly than in other species," she said.

The IGF1 gene seems particularly pliable in that regard. The research into this bit of DNA began with the Portuguese Water Dog, a shaggy, highly pedigreed breed that varies widely in size, from tiny toys to waist-high variants.

Study co-author K. Gordon Lark, professor emeritus of biology at the University of Utah, is a geneticist and owner of Mopsa, a Portuguese water dog. His team had previously scanned this breeds' genome and found a suspected locus for a "size gene" on chromosome 15.
Reaching out to other Portuguese water dog owners nationwide, the team also obtained blood samples from more than 1,000 dogs and took X-rays of 600 more.

Mopsa was "'dog number zero'" in this effort, Lark said. "She had the prototype X-rays and such so that we could see what we wanted done."

Based on the Utah findings, Ostrander and others expanded the research to include DNA from more than 3,000 dogs and 143 breeds. They finally honed in on the IGF1 gene, which appears to be regulated differently depending on a dog's size.

"This gene makes this hormone, insulin growth factor 1, that is necessary for growth," Lark explained. "The regulatory sequence determines how much of that hormone will be made and put into the dog's blood system to control the growth rate. It's like a dimmer switch for growth."
The pattern quickly became clear, Ostrander said. "Small dogs had one signature, larger breeds had another," she said.

Exceptions arose, however. For example, Rottweilers carry both the small- and big-dog signatures, although the big-body variant seems to win out, Ostrander said. Mastiffs carry both gene signatures, as well.

"That tells us that there are other genes out there that are interacting with this master-regulator, IGF1," Ostrander said.

For that reason, simply tweaking the IGF1 gene probably wouldn't lead to super-sized Chihuahuas or teacup German Shepherds.

"No, it's going to take other genes to do that," Ostrander said. "But now we know the master regulator, and we know what other kinds of genes to go after. That's what we are in the process of doing now."

More information
There's more on research into dog genetics at the Canine Health Information Center.

Sleepless Nights May Encourage Pain

(HealthDay News) -- Poor sleep can raise risks for pain in women, a new study suggests.
"This study finds that fragmented sleep profiles, akin to individuals suffering from middle of the night insomnia, health care workers on call, and parents caring for infants, alter natural systems that regulate and control pain, and can lead to spontaneous painful symptoms," researcher Michael T. Smith, of Johns Hopkins University, said in a prepared statement.

The findings are published in the April 1 issue of the journal Sleep.

The study included 32 healthy women who were studied for seven nights. For the first two nights, the women slept undisturbed for eight hours. For the next few nights, the women were then assigned to one of three groups: a control group that continued to sleep undisturbed; a forced awakening (FA) group awakened once an hour (eight times) through the night; and a restricted sleep opportunity (RSO) group subjected to partial sleep deprivation by delaying their bedtime.

On the sixth night, the women in both the FA and RSO groups underwent 36 hours of total sleep deprivation, followed by an 11-hour recovery sleep.

During the study, researchers tested the women's pain thresholds and pain inhibition. The women in the FA group showed an increase in spontaneous pain, while those in the control and RSO groups showed no changes in spontaneous pain or pain inhibition.

"Our research shows that disrupted sleep, marked by multiple prolonged awakenings, impairs natural pain control mechanisms that are thought to play a key role in the development, maintenance, and exacerbation of chronic pain," Smith said.

More information
The National Sleep Foundation has more about sleep.