Cognitive Labs

Amish barn raising from taratara 69

The Amish of Pennsylvania, according to an extensive study of 704 subjects, are 30% more likely to carry a gene known as FTO linked to obesity, along with others of similar European ancestry. This gene, which regulates a kind of protein production, is linked to food intake, and predisposes individuals to gain weight. But obesity is less of a problem with the Amish than with typical suburbanites. Why is that?

Think about getting together and framing a barn or working in the field.

It turns out brisk exercise of 3 to four hours a day shuts off the propensity to accumulate weight. It may be that this is a genetic adaptation that helped people to survive in conditions of scarcity, not unlike mutations of the APOE gene, which in its APOEe4 variant, appears to have helped children survive by metabolizing scare food supplies - with the side effect of being linked to cognitive decline in later years.

Can people go back to a nineteenth century lifestyle, when individuals were much thinner?

Not really. But they can walk or cycle on routine daily trips instead of drive, take a walk instead of watching tv, play sports such as tennis, garden, and do chores. With this level of physical activity, you could indeed consume a hearty, but not unhealthy diet and still lose weight.

Labels: amish, fto, gene

credit: Gene Expression, University of Leeds

The late summer has been a dazzling period for useful, genetic-based observations that offer insight onto disease, aging, and sociology.

1. Like a sprawling suburb, cancerous conditions result from uncontrolled cellular growth. The four genes E2f1, E2f2, and E2f3a and E2f3b work as a quartet to regulate cellular growth. Understanding the interdependency between these genes may shed light on cancer's preconditions.

2. Children of older fathers are much more likely to be bipolar, according to the statistics, possibly a result of slight flaws introduced into the sperm of men as they age. The older the father, the greater the incidence of bipolarity compared to a control population.

3. The vasopressin receptor 1a gene governs relative 'commitment' in male voles (and probably humans)...

Labels: bipolar, e2f1, gene, genes, vassopressin

...Scientists said on Sunday they have pinpointed a new gene linked to
Alzheimer's disease, the incurable brain disorder that is the top cause of dementia in the elderly.

Abnormalities in a gene called SORL1 increased the risk for the disease, and this finding could help scientists develop new treatments, the researchers reported in the journal Nature Genetics.

The researchers looked at DNA samples from 6,000 people from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs. They found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.

The late-onset form, affecting people age 65 and up, represents about 90 percent of Alzheimer's cases. The rarer early-onset form affects people from about age 30 to 65.

Only one other gene, called ApoE4, has been identified as a risk factor for late-onset Alzheimer's. It was identified in 1993.

Several genes are linked with early Alzheimer's, and study of both types might lead to better understanding of how the disease begins and how to tackle it.

Many scientists think Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that clumps together to form plaques. That material stems from a protein called amyloid precursor protein, or APP.

SORL1 controls the distribution of APP inside nerve cells of the brain. When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.

Alzheimer's is a complex disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Scientists have struggled to understand the biology of the disease and its genetic and environmental causes.

'PIECE OF THE PUZZLE'

"It's another clue to the way in which this disease comes about, another piece of the puzzle," Dr. Peter St. George-Hyslop, director of the Center for Research in Neurodegenerative Diseases at the University of Toronto and one of the key researchers, said in a telephone interview.

"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.

St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.

"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Center in New York, also involved in the research, said in a statement.

The disease first affects parts of the brain controlling memory and thinking, but as it advances it kills cells elsewhere in the brain. Eventually, if the patient has no other serious illness, the loss of brain function will prove fatal.

Researchers from Boston University and the Mayo Clinic College of Medicine in Jacksonville, Florida, also took part in the five-year study.

Labels: alzheimers, apoe, gene, sorl

A new study at the Albert Einstein College of Medicine has linked a gene that helps people live longer to increased mental ability and delayed onset of Alzheimer's Disease.

The study is published in the current issue of Neurology and was conducted by researchers at the Albert Einstein College of Medicine of Yeshiva University in the Bronx, New York, and forms part of the Longevity Genes Project.

Dr Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine, and his team looked at 158 people who were aged 95 and over and descended from Ashkenazi Jews who originally came from Eastern Europe. They asked this group, and another group of people of the same age who were not of Ashkenazi descent to complete cognitive tests of mental ability.

The scientists found that those who completed the test successfully (by correctly answering 25 of thirty questions) were two to three times more likely to possess the W variant of the CETP gene than those who did not.

In a later study the researchers examined a group of 124 people also of Ashkenazi descent, aged between 75 and 85. In this study they found that the ones who did not develop dementia on follow up were five times more likely to have the CETP W gene than those who did not.

The researchers chose to look at Ashkenazi people because they came from a small number of ancestors, making it easier to detect the differences in the genetic make up of the individuals due to the more uniform nature of their genetic patterns compared to the public at large.

This research comes on top of earlier studies, also by Dr. Barzilai and his team where they first showed that CETP W helps people live longer and also pass this gene onto their descendants. This study suggested that CETP W changes the size of good (HDL) and bad (LDL) cholesterol molecules in the blood - which helps people live longer because the smaller ones get stuck in the blood vessels more easily, leading to clots.

The centenarians in that study were three times more likely to have the CETP W variant and also had the larger HDL and LDL cholesterol molecules in their blood.

This latest study suggests that the cholesterol changing properties of CETP W may be protecting mental function by preventing the build up of cholesterol in the brain's blood vessels, thus reducing strokes and heart attacks, or by some other means that is yet to be discovered.

“Without good brain function, living to age 100 is not an attractive proposition,” says Dr. Barzilai in a press release. “We’ve shown that the same gene variant that helps people live to exceptional ages has the added benefit of helping them think clearly for most of their long lives."

In the population at large, the chances of living to 100 is one in 10,000. The Ashkenazi population has a strong family history of longevity. Dr Barzilai pointed out that the odds of living much longer are much increased if you already have a centenarian in your family, and it is not necessarily lifestyle related. Many of the long living Ashkenazis are not vegetarian or athletic, and some of them have smoked for 90 years.

Cholesterol is an essential molecule for building cells. High levels of oxidized LDL cholesterol is thought to thicken artery walls (atherosclerosis) and increases risk of heart diseases. HDL cholesterol and the larger HDL in particular is thought to help remove cholesterol from thickened artery walls and high levels of HDL are linked to lower incidence of atherosclerosis and may even help to reverse the condition.

Labels: alzheimers, brain, CETP W, gene