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Abnormally interacting neurons might be the reason for cognitive deficits in Fragile X syndrome (FXS

Dr Andre Fenton and colleagues from the New York University have discovered that in FXS which is responsible for the most widespread form of autism is characterized by normally functioning neurons for cognition and memory. However, the problem lies in the failure of these neurons interacting correctly which might result in long-term cognitive deficits. The study was conducted in mice which have genetic defects in the FMR1 gene similar to that seen in a human patient. This could have therapeutic implications since one can now target neuronal interactions instead of the upstream molecular abnormalities caused by the mutation.

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