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New drug 'reverses Fragile X syndrome symptoms'

Washington, Thu, 12 Apr 2012 ANI
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Washington, Apr 12 (ANI): A new compound reverses many of the major symptoms associated with Fragile X syndrome (FXS), which is the most common form of inherited intellectual disability and a leading cause of autism, a new study has claimed.

The paper describes the exciting observation that the FXS correction can occur in adult mice, after the symptoms of the condition have already been established.

Fragile X patients suffer from a complex set of neuropsychiatric symptoms of varying severity which include anxiety, hyperactivity, learning and memory deficits, low IQ, social and communication deficits, and seizures.

Previous research has suggested that inhibition of mGlu5, a subtype of receptor for the excitatory neurotransmitter glutamate, may be useful for ameliorating many of the major symptoms of the disease.

The new study, a collaboration between a group at F. Hoffmann-La Roche Ltd. in Switzerland, led by Lothar Lindemann, and a group at the Picower Institute for Learning at the Massachusetts Institute of Technology, led by Mark Bear, used a newly developed mGlu5 inhibitor called CTEP to examine whether pharmacologic inhibition of mGlu5 could reverse FXS symptoms.

The researchers used a mouse model of FXS and administered CTEP after the brain had matured.

"We found that even when treatment with CTEP was started in adult mice, it reduced a wide range of FXS symptoms, including learning and memory deficits and auditory hypersensitivity, as well as morphological changes and signalling abnormalities characteristic of the disease," Lindemann said.

Although the CTEP drug itself is not being developed for humans, the findings have significance for human FXS.

"The most important implications of our study are that many aspects of FXS are not caused by an irreversible disruption of brain development, and that correction of the altered glutamate signaling can provide widespread therapeutic benefit," Bear said.

The study has been recently published in the journal Neuron. (ANI)

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