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Vol. LXIV, No. 10
May 11, 2012
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Digest

Agent Reduces Autism-Like Behaviors in Mice

NIH researchers have reversed behaviors in mice resembling two of the three core symptoms of autism spectrum disorders (ASD). An experimental compound, called GRN-529, increased social interactions and lessened repetitive self-grooming behavior in a strain of mice that normally display such autism-like behaviors, the researchers say.

GRN-529 is a member of a class of agents that inhibit activity of a subtype of receptor protein on brain cells for the chemical messenger glutamate, which are being tested in patients with an autism-related syndrome. Although mouse brain findings often don’t translate to humans, the fact that these compounds are already in clinical trials for an overlapping condition strengthens the case for relevance, according to the researchers.

“Our findings suggest a strategy for developing a single treatment that could target multiple diagnostic symptoms,” explained Dr. Jacqueline Crawley of the National Institute of Mental Health. “Many cases of autism are caused by mutations in genes that control an ongoing process—the formation and maturation of synapses, the connections between neurons. If defects in these connections are not hard-wired, the core symptoms of autism may be treatable with medications.”

Crawley, Dr. Jill Silverman and colleagues at NIMH and Pfizer Worldwide Research and Development, Groton, Conn., reported their discovery Apr. 25 in the journal Science Translational Medicine.

“These new results in mice support NIMH-funded research in humans to create treatments for the core symptoms of autism,” said NIMH director Dr. Thomas Insel. “While autism has been often considered only as a disability in need of rehabilitation, we can now address autism as a disorder responding to biomedical treatments.”

Test Links Strains of Common Parasite to Severe Illness in Newborns

Scientists have identified which strains of the Toxoplasma gondii parasite, the cause of toxoplasmosis, are most strongly associated with premature births and severe birth defects in the United States
Scientists have identified which strains of the Toxoplasma gondii parasite, the cause of toxoplasmosis, are most strongly associated with premature births and severe birth defects in the United States

Scientists have identified which strains of the Toxoplasma gondii parasite, the cause of toxoplasmosis, are most strongly associated with premature births and severe birth defects in the United States. The researchers used a new blood test developed by scientists at the National Institute of Allergy and Infectious Diseases to pinpoint T. gondii strains that children acquire from their acutely infected mothers while in the womb.

Pregnant women can become infected with T. gondii through contact with cat feces that contain infectious forms of the parasite or by eating undercooked meat. Women who become infected while pregnant may miscarry, give birth prematurely or have babies with eye or brain damage.

“If undetected or untreated, congenital toxoplasmosis can have serious consequences for a child’s quality of life,” noted NIAID director Dr. Anthony Fauci. “The findings from this study support the value of screening for toxoplasmosis to identify patients who could benefit from treatment.”

Currently available blood tests can determine whether a person has ever been infected with any strain of Toxoplasma parasite. The experimental test developed at NIAID improves upon the older tests because it can detect the presence of strain-specific antibodies that distinguish infecting strains from one another.

The test was developed by Dr. Michael Grigg of NIAID’s Laboratory of Parasitic Diseases and his colleagues. The new study was published online in Clinical Infectious Diseases.

Brain-Activated Muscle Stimulation Restores Monkeys’ Hand Movement

An artificial connection between the brain and muscles can restore complex hand movements in monkeys following temporarily induced paralysis, according to a study funded by NIH.

In a report in the journal Nature, researchers describe how they combined two pieces of technology to create a “neuroprosthesis,” a device that replaces lost or impaired nervous system function.

One piece is a multi-electrode array implanted directly into the brain that serves as a brain-computer interface. The array allows researchers to detect the activity of about 100 brain cells and decipher the signals that generate arm and hand movements. The second piece is a functional electrical stimulation (FES) device that delivers electrical current to the paralyzed muscles, causing them to contract. The brain array activates the FES device directly, bypassing the spinal cord to allow intentional, brain-controlled muscle contractions and restore movement.

The research team was led by Dr. Lee E. Miller, professor of physiology at Northwestern University’s Feinberg School of Medicine. This new research moves beyond earlier work from his group showing that a similar neuroprosthesis restores monkeys’ ability to flex or extend the wrist despite paralysis.

“With these neural engineering methods, we can take some of the important basic physiology that we know about the brain and use it to connect the brain directly to muscles,” he said. “This connection from brain to muscles might someday be used to help patients paralyzed due to spinal cord injury perform activities of daily living and achieve greater independence.”


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