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D-Cyclosrine may improve socialbility for autistic spectrum disability

Clinical trials to start using D-Cyclosrine to treat socialibility dificulties.

NORFOLK, Va., Dec. 11 (UPI) — A U.S. researcher says a possible drug to treat impaired sociability in those with autism may be a breakthrough.

Dr. Stephen Deutsch of Eastern Virginia Medical School in Norfolk says the novel treatment strategy will soon be entering the clinical trial phase.

“Persons with autism spectrum disorders are either disinterested in social interactions or find them unpleasant. They often don’t understand what other people are thinking or feeling and misinterpret social cues,” Deutsch says in a statement. “Sadly, persons with autism spectrum disorders are often painfully aware of their limited sociability, which can lead to profound feelings of sadness and frustration.”

Deutsch and colleagues have used mouse studies — in particular a strain of mouse with limited sociability who — unlike normal mice — create distance with other mice to avoid social contact to test the drug.

The medication originally developed to treat tuberculosis but known to affect social behavior — called D-Cycloserine seems to address deficits of sociability in the socially deficient mice — the mice behave as a normal mice would when placed near another mouse.

Deutsch is scheduled to present the findings at Eastern Virginia Medical School’s Quarterly Autism Education Series.

An analogue of the amino acid D-alanine with broad-spectrum antibiotic and glycinergic activities. D-cycloserine interferes with bacterial cell wall synthesis by competitively inhibiting two enzymes, L-alanine racemase and D-alanine:D-alanine ligase, thereby impairing peptidoglycan formation necessary for bacterial cell wall synthesis. This agent may be bactericidal or bacteriostatic, depending on its concentration at the infection site and the susceptibility of the organism. In addition, D-cycloserine is an excitatory amino acid and partial agonist at the glycine binding site of the NMDA receptor in the central nervous system (CNS); binding to the central NMDA receptor may result in amelioration of neuropathic pain.

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