Normally, when people discuss the benefits of exercise, they focus on how it affects the body physically – stronger muscles, trimmer stomach, and so forth.

However, a new study suggests a good aerobic workout may actually have mental benefits as well.

Researchers have demonstrated that regularly engaging in aerobic exercise can increase the size of the hippocampus, which is important for memory and spatial navigation, in adults ages 55 to 80, and perhaps even shave the risk of dementia.

The hippocampus tends to shrink in size as people age, which can negatively affect memory.

For the study, researchers recruited 120 older people who did not exercise on a regular basis and randomly assigned them to one of two programs: either an aerobic exercise program, in which participants walked around a track for 40 minutes three days a week, or a stretching-and-weights program.

The group assigned to the aerobic exercise program showed a volume increase of 2.12 percent in the left hippocampus and 1.97 percent in the right hippocampus.  Meanwhile, the group assigned to the stretching program decreased in hippocampus volume by 1.40 percent on the left and 1.43 percent on the right.

The study was published in Proceedings of the National Academy of Sciences.

A new peptide may offer relief for people who suffer from chronic pain, according to a new study.

And unlike current treatments, the peptide does not appear to have adverse side effects such as reduced motor coordination, memory loss or depression.

Indiana University School of Medicine researchers discovered the peptide, CBD3, which has been shown in mice to interfered with signals that navigate calcium channels to produce pain.

Most current treatments to block pain signals inhibit the influx of calcium, which is responsible for regulating heart rhythm and vital functions in other organs.  CBD3 instead binds to the calcium channel to reduce pain signals without interrupting calcium flow.

This makes CBD3 a potentially safer treatment than addictive opioids or an analgesic called Prialt that is injected into the spinal column, according to researchers.  Both opioids and Prialt can cause respiratory distress, cardiac irregularities and other problems.

The researchers hope their finding will herald a new gold standard for the control of chronic pain, which affects over 76 million Americans a year, according to the National Centers for Health Statistics.

The study was published in Nature Medicine.

Sometimes, it comes down to a single gene.

In 1993, researchers discovered a gene known as ApoE4 — carried by about a quarter of the population — that triples the risk for getting Alzheimer’s. In 2009, three more risky genes were discovered, and one of them, called clusterin, or CLU, was found to increase the risk of getting Alzheimer’s by another 16 percent.

But until now, the exact function of the CLU gene was unknown.  However, UCLA researchers recently have discovered that this particular risk gene begins to damage the brain 50 years before people normally get Alzheimer’s.

Paul Thompson, a UCLA professor of Neurology, and his team, have found that CLU impairs the development of myelin, which is the protective covering around the neuron’s axons in the brain.  This makes the brain weaker and more vulnerable to the onset of Alzheimer’s later in life.

The researchers scanned the brains of nearly 400 healthy adults aged 20 to 30 by using a newer type of MRI that maps the brain’s connections.  They compared the brains of people who carried the risky variant of CLU against those who carried a different variant.

They found that those who carried the risky variant had lower white matter integrity, which may increase vulnerability to developing Alzheimer’s.

While Alzheimer’s has traditionally been considered as a disease marked by neuron loss and widespread gray matter atrophy, according to Thompson, this study shows that the destruction of myelin in white-matter brain pathways is also a key component of disease development.

According to researchers, 88 percent of Caucasians carry the CLU gene.  The other 12 percent are considered to have an ‘Alzheimer’s resistance gene’ that protects their brain wiring.

The researchers hope that knowing the role of the gene will prove useful in predicting people’s risk of developing Alzheimer’s and taking preventative steps in protecting the brain 50 years before the disease’s onset, long before symptoms ever develop.

“We know that many lifestyle factors, such as regular exercise and a healthful diet, may reduce the risk of cognitive decline, particularly in those genetically at risk for Alzheimer’s, so this reminds us how important that is,” Thompson said in a press release.

In the largest study of its kind, researchers have identified four new genes linked to late-onset Alzheimer’s disease, the most common form of dementia. An additional study has confirmed a previously identified gene and found a fifth, USA Today reported.

In the first study, researchers compiled and analyzed genetic data from 54,000 individuals – about a third whom had Alzheimer’s and the rest of whom did not – to identify the four new genes.

The study was conducted by scientists from 45 universities and research institutes in the United States.  Collectively, the group was called the Alzheimer’s disease Genetics Consortium.  The research was funded by the National Institutes of Health.

Later, the consortium also helped to identify a fifth gene, which was reported in the second study by scientists from the U.S., the United Kingdom, France and other European countries.

“I’ve been in Alzheimer’s genetics since 1985, and I would have to say this is the most exciting event that’s happened,” said lead author of the first study Gerard Schellenberg, professor in the Department of Pathology and Laboratory Medicine at the University of Pennsylvania School of Medicine, in Philadelphia.  “Up until this point, there have only been five known genes for Alzheimer’s risk, and so we’ve essentially doubled the genes people know about.”

Finding new genes is essential, according to Schellenberg, because each gene is a clue as to what causes the degenerative disease.  The researchers hope their findings will help scientists develop new drugs and identify high-risk individuals.

“The brain is like a black box. You can do some imaging when patients are alive, and poke around after someone dies, to try to figure out why someone has Alzheimer’s or not,” but the new findings may increase the ability to predict who will get it, Schellenberg said.

Currently, treatments for Alzheimer’s are limited, and there is no prevention or cure for the disease.

Many of the genetic researchers involved with these studies are planning an even larger, similar study in the future, called the International Genomics of Alzheimer’s Project.

Both studies were published in the journal Nature Genetics.

Click here to read more from USA Today.

As the number of people suffering from Alzheimer’s disease climbs, so does the number of unpaid caregivers, USA Today reported.

According to the Alzheimer’s Association, there are nearly 15 million unpaid caregivers in the United States who are helping people who have Alzheimer’s or other forms of dementia – a 37 percent increase from last year.

About 5.4 million people currently have Alzheimer’s, a condition linked with aging.  Every 69 seconds, someone else develops it.

The family members and friends responsible for them provide about 17 billion hours of unpaid care, valued at 202.6 billion.

“The toll on families is devastating,” says the association’s Beth Kallmyer, senior director of constituent services. “Stress is extremely high, and one-third are experiencing depression.”

Alzheimer’s is the sixth-leading cause of death in the US, and out of the top ten, it is the only one that has no prevention or cure.

The burden on family might be eased if people were more aware of early symptoms and were diagnosed sooner, suggested Beth Kallmyer, senior director of constituent services at the Alzheimer’s Association.

“This disease is never going to be easy, but empowering patients to make financial and long-term care decisions early helps families,” she says.

Click here to read more from USA Today.

Researchers at the Fisher Center for Alzheimer’s Research Foundation have discovered a protein that spurs the onset of Alzheimer’s disease.

Dr. Paul Greengard, Nobel Laureate and Director of the Fisher Center for Alzheimer’s Research laboratory, and his team at The Rockefeller University have identified a protein called gamma-secretase activating protein (gSAP), which stimulates the production of beta-amyloid.

Beta-amyloid is a substance that becomes toxic in Alzheimer’s disease and is responsible for most of the symptoms of the disease, such as memory loss.

The researchers also discovered that an anti-cancer drug, Gleevec, targets gSAP and consequently lowers beta-amyloid levels in the brain.

Moreover, inhibiting the function of gSAP is not toxic to nervous cells, unlike other beta-amyloid inhibitor drugs which often produce severe toxic reactions.

With this discovery, Greengard hopes to usher in a new era of development for Alzheimer’s drugs.

“Millions of people suffer from Alzheimer’s disease, and the treatment options are limited,” Greengard said.  “Existing drugs may mask symptoms for a time but do nothing to stop the relentless downward progression of Alzheimer’s.  What is needed are safe and effective medications that will halt the cause of the underlying disease.  It is our hope that this gSAP protein will greatly add to the creation of safe and effective Alzheimer’s treatment.”

The study was published in the journal Nature.