Year: 2012 (page 11 of 55)

misfolded synuclein leads to parkinson’s spread

Image of a stained Lewy body

Research from my alma mater, The University of Pennsylvania, reveals some details on how Parkinson’s disease spreads throughout neural cells. The research led by Virginia Lee in the Department of Pathology and Laboratory Medicine has found that the protein α-synuclein plays a key role. When it is misfolded it passes through neural cells and causes cellular death and the formation of Lewy bodies. From Scientific American:

Parkinson’s disease has two distinct features: clumps of protein called Lewy bodies and a dramatic loss of nerve cells that produce the chemical messenger dopamine. When Lee’s team injected the misfolded α-synuclein into a part of the mouse brain rich in dopamine-producing cells, Lewy bodies began to form. This was followed by the death of dopamine neurons. Nerve cells that linked to those near the injection site also developed Lewy bodies, a sign that cell-to-cell transmission was taking place, say the researchers.

Greenamyre says that that is possible, but hasn’t yet been proved. “All of the cells affected in this paper were those directly in contact with the injection site,” he says.

Nevertheless, within six months of the injection, coordination of movement, grip strength and balance had all deteriorated in the mice, echoing what happens in people with Parkinson’s disease.

“It’s really pretty extraordinary,” says Eliezer Masliah, a neuroscientist at the University of California, San Diego. “We have been trying that experiment for a long time in the lab and we have not seen such dramatic effects.” The study lends theoretical support to the handful of biotechnology companies that are sponsoring clinical trials of α-synuclein antibodies for Parksinson’s, Masliah says. It should also spur research on how the protein gets in and out of cells, he adds.

Check out the details of the research in Science.

telomere length linked to longevity

Telomere length has long been thought to play a role in the death of cells. Our telomeres shorten as we age, and the truncated telomeres have been linked to some diseases. Now research suggests that it increases overall chances of dying soon. From Science News:

To find out, researchers at Kaiser Permanente and the University of California, San Francisco measured telomere length in 110,266 people in northern California. The participants are part of an ongoing project that explores links between genetics and health. This study is the largest ever to examine telomeres’ role in health.

The 10 percent of people with the shortest telomeres had a more than 20 percent higher risk of dying than people with longer telomeres, Catherine Schaefer, an epidemiologist who directs the Kaiser Permanente Research Program on Genes, Environment and Health, reported November 8 at the annual meeting of the American Society of Human Genetics. “It seems as though once your telomeres get critically short, your risk of dying goes up,” she said. The increased death risk is about the same as for people who drink 20 to 30 alcoholic beverages per week or smoke for 20 to 30 years. “It’s a modest increase, but it’s not nothing.”

The study was presented at the American Society of Human Genetics annual meeting.

how camels survive in the desert

An Arabian Camel

Genomic studies are helping researchers determine what is unique about these dessert dwelling mammals. It turns out it is mostly their metabolism. From Scientific American:

Camels, as ruminants like cattle and sheep, digest food by chewing the cud. But many of the Bactrian genome’s rapidly evolving genes regulate the metabolic pathway, suggesting that what camels do with the nutrients after digestion is a whole different ball game. “It was surprising to me that they had significant difference in the metabolism,” says Kim Worley, a molecular geneticist at Baylor College of Medicine in Houston, Texas. The differences could point to how Bactrians produce and store energy in the desert.

The work shows that camels can withstand massive blood glucose levels owing in part to changes in genes that are linked to type II diabetes in humans. The Bactrians’ rapidly evolving genes include some that regulate insulin signaling pathways, the authors explain. A closer study of how camels respond to insulin may help to unravel how insulin regulation and diabetes work in humans. “I’m very interested in the glucose story,” says Brian Dalrymple, a computational biologist at the Queensland Bioscience Precinct in Brisbane, Australia.

The researchers also identified sections of the genome that could begin to explain why Bactrian camels are much better than humans at tolerating high levels of salt in their bloodstreams. In humans, the gene CYP2J controls hypertension: suppressing it leads to high blood pressure. However, camels have multiple copies of the gene, which could keep their blood pressure low even when they consume a lot of salt, suggest the authors of the latest work.

The study appears in Nature Communications.

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