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Vol. LXV, No. 11
May 24, 2013
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Digest

Study Provides Clarity on Supplements to Protect Against Blinding Eye Disease

Adding omega-3 fatty acids did not improve a combination of nutritional supplements commonly recommended for treating age-related macular degeneration (AMD), a major cause of vision loss among older Americans, according to a study from the National Eye Institute. The plant-derived antioxidants lutein and zeaxanthin also had no overall effect on AMD when added to the combination; however, they were safer than the related antioxidant beta-carotene, according to the study published online May 5 in the Journal of the American Medical Association.

The Age-Related Eye Disease Study (AREDS), which was led by NEI and concluded in 2001, established that daily high doses of vitamins C and E, beta-carotene and the minerals zinc and copper—called the AREDS formulation—can help slow the progression to advanced AMD. The American Academy of Ophthalmology now recommends use of the AREDS formulation to reduce the risk of advanced AMD. However, beta-carotene use has been linked to a heightened risk of lung cancer in smokers. And there have been concerns that the high zinc dose in AREDS could cause minor side effects, such as stomach upset, in some people.

In 2006, NEI launched AREDS2, a 5-year study designed to test whether the original AREDS formulation could be improved by adding omega-3 fatty acids; adding lutein and zeaxanthin; removing beta-carotene; or reducing zinc. The study also examined how different combinations of the supplements performed. Omega-3 fatty acids are produced by plants, including algae, and are present in oily fish such as salmon. Lutein and zeaxanthin are carotenoids, a class of plant-derived vitamins that includes beta-carotene; both are present in leafy green vegetables and, when consumed, they accumulate in the retina. Prior studies had suggested that diets high in lutein, zeaxanthin and omega-3 fatty acids protect vision.

Womenís, Menís Brains Respond Differently to Hungry Infantís Cries

Photo of woman on bed trying to calm her infant crying

Researchers at NIH have uncovered firm evidence for what many mothers have long suspected: women’s brains appear to be hard-wired to respond to the cries of a hungry infant.

Researchers asked men and women to let their minds wander, then played a recording of white noise interspersed with the sounds of an infant crying. Brain scans showed that, in the women, patterns of brain activity abruptly switched to an attentive mode when they heard the infant cries, whereas the men’s brains remained in the resting state. The findings appear in NeuroReport.

“Previous studies have shown that, on an emotional level, men and women respond differently to the sound of an infant crying,” said study co-author Dr. Marc Bornstein, head of the child and family research section of NICHD, which conducted the study. “Our findings indicate that men and women show marked differences in terms of attention as well.”

Earlier studies showed that women are more likely than men to feel sympathy when they hear an infant cry and are more likely to want to care for the infant.

Study Uses Botox to Find New Wrinkle in Brain Communication

NINDS researchers used the popular anti-wrinkle agent Botox to discover a new and important role for a group of molecules that nerve cells use to quickly send messages. This novel role for the molecules, called SNAREs, may be a missing piece that scientists have been searching for to fully understand how brain cells communicate under normal and disease conditions.

Every day, almost 100 billion nerve cells throughout the body send thousands of messages through nearly 100 trillion communication points called synapses. Cell-to-cell communication at synapses controls thoughts, movements and senses and could provide therapeutic targets for a number of neurological disorders, including epilepsy.

Nerve cells use chemicals, called neurotransmitters, to rapidly send messages at synapses. Like pellets inside shotgun shells, neurotransmitters are stored inside spherical membranes, called synaptic vesicles. Messages are sent when a carrier shell fuses with the nerve cell’s own shell, called the plasma membrane, and releases the neurotransmitter “pellets” into the synapse.

SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) are three proteins known to be critical for fusion between carrier shells and nerve cell membranes during neurotransmitter release.

“Without SNAREs there is no synaptic transmission,” said Dr. Ling-Gang Wu of NINDS.

Botulinum toxin, or Botox, disrupts SNAREs. In a study published in Cell Reports, Wu and his colleagues describe how they used Botox and similar toxins as tools to show that SNAREs may also be involved in retrieving message carrier shells from nerve cell membranes immediately after release.


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