Health for life

Widely available in pharmacies and health stores, phosphatidylserine is a natural food supplement produced from beef, oysters, and soy. Proven to improve cognition and slow memory loss, its a popular treatment for older people experiencing memory impairment. Now a team headed by Prof. Gil Ast and Dr. Ron Bochner of Tel Aviv Universitys Department of Human Molecular Genetics has discovered that the same supplement improves the functioning of genes involved in degenerative brain disorders, including Parkinsons disease and Familial Dysautonomia (FD).

In FD, a rare genetic disorder that impacts the nervous system and appears almost exclusively in the Ashkenazi Jewish population, a genetic mutation prevents the brain from manufacturing healthy IKAP proteins — which likely have a hand in cell migration and aiding connections between nerves — leading to the early degeneration of neurons. When the supplement was applied to cells taken from FD patients, the gene function improved and an elevation in the level of IKAP protein was observed, reports Prof. Ast. These results were replicated in a second experiment which involved administering the supplement orally to mouse populations with FD.

The findings, which have been published in the journal Human Molecular Genetics, are very encouraging, says Prof. Ast. "That we see such an effect on the brain — the most important organ in relation to this disease — shows that the supplement can pass through the blood-brain barrier even when administered orally, and accumulate in sufficient amounts in the brain."

Slowing the death of nerve cells

Already approved for use as a supplement by the FDA, phosphatidylserine contains a molecule essential for transmitting signals between nerve cells in the brain. Prof. Ast and his fellow researchers decided to test whether the same chemical, which is naturally synthesized in the body and known to boost memory capability, could impact the genetic mutation which leads to FD.

Researchers applied a supplement derived from oysters, provided by the Israeli company Enzymotec, to cells collected from FD patients. Noticing a robust effect on the gene, including a jump in the production of healthy IKAP proteins, they then tested the same supplement on mouse models of FD, engineered with the same genetic mutation that causes the disease in humans.

The mice received the supplement orally, every two days for a period of three months. Researchers then conducted extensive genetic testing to assess the results of the treatment. "We found a significant increase of the protein in all the tissues of the body," reports Prof. Ast, including an eight-fold increase in the liver and 1.5-fold increase in the brain. "While the food supplement does not manufacture new nerve cells, it probably delays the death of existing ones," he adds.

Therapeutic potential for Parkinsons

That the supplement is able to improve conditions in the brain, even when given orally, is a significant finding, notes Prof. Ast. Most medications enter the body through the blood stream, but are incapable of breaking through the barrier between the blood and the brain.

In addition, the researchers say the supplements positive effects extend beyond the production of IKAP. Not only did phosphatidylserine impact the gene associated with FD, but it also altered the level of a total of 2400 other genes — hundreds of which have been connected to Parkinsons disease in previous studies.

The researchers believe that the supplement may have a beneficial impact on a number of degenerative diseases of the brain, concludes Prof. Ast, including a major potential for the development of new medications which would help tens of millions of people worldwide suffering from these devastating diseases.

Research has shown that exercise is good for the brain. Now investigators have identified a molecule called irisin that is produced in the brain during endurance exercise and has neuroprotective effects. Researchers were able to artificially increase the levels of irisin in the blood to activate genes involved in learning and memory. The findings, published online October 10 in the Cell Press journal Cell Metabolism, may be useful for designing drugs that utilize this exercise-induced molecule to guard against neurodegenerative diseases and improve cognition in the aging population.

While its known that exercise can boost cognitive function and lessen symptoms of neurological diseases like depression, stroke, and Alzheimers disease, the mechanisms underlying these effects are unclear. One important player is thought to be a growth factor named brain-derived neurotrophic factor (BDNF).

Through experiments conducted in mice, investigators led by Dr. Bruce Spiegelman of the Dana-Farber Cancer Institute and Harvard Medical School found that a molecule called FNDC5 and its cleavage product, irisin, are elevated by endurance exercise in the brain and increase BDNF expression. On the other hand, mice genetically altered to have low irisin levels in the brain had reduced levels of BDNF.

The team also found that raising levels of irisin in the circulation caused the molecule to cross the blood brain barrier, where it increased expression of BDNF and activated genes involved in cognition.

"Our results indicate that FNDC5/irisin has the ability control a very important neuroprotective pathway in the brain," says Dr. Spiegelman. The researchers next plan to work on developing a stable form of the irisin protein that can be given to mice by injection and may augment the brains natural anti-degeneration pathways.

Exercising regularly in old age may better protect against brain shrinkage than engaging in mental or social activities, according to a new study published in the October 23, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology. Research suggests that brain shrinkage may lead to problems with memory and thinking.

"People in their seventies who participated in more physical exercise, including walking several times a week, had less brain shrinkage and other signs of aging in the brain than those who were less physically active," said study author Alan J. Gow, PhD, with the University of Edinburgh in Scotland. "On the other hand, our study showed no real benefit to participating in mentally and socially stimulating activities on brain size, as seen on MRI scans, over the three-year time frame."

Researchers looked at medical records of 638 people from Scotland born in 1936. The participants were given MRI scans at 73 years old.

The group gave details about their exercise habits, ranging from moving only in connection with necessary household chores to keeping fit with heavy exercise or participating in competitive sports several times per week. They also reported their participation in social and mentally stimulating activities.

The study found that after three years, people who participated in more physical activity experienced less brain shrinkage than those who exercised minimally.

"Our results show that regularly exercising in old age is potentially important to protecting the brain as we age," said Gow.

(Article first published as Acai and the Berry Family Promote Health for the New Year on Technorati.)
Each day our cells are bombarded with negatively charged ions known as free radicals that cause damage leading to accelerated aging and increased risk of heart disease, cancer and dementia. It`s estimated that each of our trillion or so cells is assaulted by up to 10,000 free radicals each day.