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Vol. LXV, No. 19
September 13, 2013
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Digest

Researchers Find Essential Brain Circuit in Visual Development

A study in mice reveals an elegant circuit within the developing visual system that helps dictate how the eyes connect to the brain. The research has implications for treating amblyopia, a vision disorder that occurs when the brain ignores one eye in favor of the other.

A study in mice reveals an elegant circuit within the developing visual system that helps dictate how the eyes connect to the brain. The research has implications for treating amblyopia, a vision disorder that occurs when the brain ignores one eye in favor of the other.

A study in mice reveals an elegant circuit within the developing visual system that helps dictate how the eyes connect to the brain. The research, funded by NIH, has implications for treating amblyopia, a vision disorder that occurs when the brain ignores one eye in favor of the other.

Amblyopia is the most common cause of visual impairment in childhood and can occur whenever there is a misalignment between what the two eyes see—for example, if one eye is clouded by a cataract or if the eyes are positioned at different angles. The brain at first has a slight preference for the more functional eye, and over time—as that eye continues to send the brain useful information—the brain’s preference for that eye gets stronger at the expense of the other eye.

Patching the strong eye can help correct amblyopia. But if the condition isn’t caught and corrected during childhood, visual impairment in the weaker eye is likely to persist into adulthood.

“Our study identifies a mechanism for visual development in the young brain and shows that it’s possible to turn on the same mechanism in the adult brain, thus offering hope for treating older children and adults with amblyopia,” said Dr. Joshua Trachtenberg, associate professor of neurobiology at David Geffen School of Medicine, University of California, Los Angeles. The study was published in Nature.

Single Gene Change Increases Mouse Lifespan By 20 Percent

By lowering the expression of a single gene, researchers at NIH have extended the average lifespan of a group of mice by about 20 percent—the equivalent of raising the average human lifespan by 16 years, from 79 to 95. The research team targeted a gene called mTOR, which is involved in metabolism and energy balance, and may be connected with the increased lifespan associated with caloric restriction.

A detailed study of these mice revealed that gene-influenced lifespan extension did not affect every tissue and organ the same way. For example, the mice retained better memory and balance as they aged, but their bones deteriorated more quickly than normal.

This study appeared in the Aug. 29 edition of Cell Reports.

“While the high extension in lifespan is noteworthy, this study reinforces an important facet of aging; it is not uniform,” said lead researcher Dr. Toren Finkel of the National Heart, Lung, and Blood Institute. “Rather, similar to circadian rhythms, an animal might have several organ-specific aging clocks that generally work together to govern the aging of the whole organism.”

Finkel, who heads NHLBI’s Laboratory of Molecular Biology, noted that these results may help guide therapies for aging-related diseases that target specific organs, such as Alzheimer’s. However, further studies in these mice as well as human cells are needed to identify exactly how aging in these different tissues is connected at the molecular level.

Investigational Oral Regimen for Hepatitis C Shows Promise

In a study of an all-oral drug regimen, a majority of volunteers with liver damage due to hepatitis C virus (HCV) infection were cured following a 6-month course of therapy that combined an experimental drug, sofosbuvir, with the licensed antiviral drug ribavirin. The results showed that the regimen was highly effective in clearing the virus and well tolerated in a group of patients who historically have had unfavorable prognoses.

Scientists from NIAID and the Clinical Center led the phase II trial. The findings appeared in the Aug. 28 issue of the Journal of the American Medical Association.

More than 3 million Americans have chronic HCV infection, a condition that is a major cause of cirrhosis (liver tissue scarring) and liver cancer and a leading reason for liver transplantation. Deaths from HCV-related liver disease number about 15,000 every year. Standard treatment for HCV can last up to a year and usually involves weekly injections of pegylated interferon-alpha given with the oral drug ribavirin and an HCV protease inhibitor. Side effects from this treatment can be severe, notably from interferon-alpha, and can include depression, flu-like symptoms and anemia.

“There is a pressing need for hepatitis C virus treatments that are less burdensome to the patient, have fewer side effects and take less time to complete. Building on previous work, this trial provides compelling evidence that interferon-free regimens can be safe and effective,” said NIAID director and study co-author Dr. Anthony Fauci.


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