Fragile X Finding Shows Normal Neurons that Interact Poorly
Neurons in mice afflicted with the genetic defect that causes Fragile X syndrome (FXS) appear similar to those in healthy mice, but these neurons fail to interact normally, resulting in the long-known cognitive impairments, shows a new study by a team of neuroscientists.
The results point to a new approach to address FXS: targeting neuronal interactions rather than the immediate molecular abnormalities of genetic mutations.
“The genetic defect that causes the most widespread form of intellectual disability and autism is surprisingly characterized by normally functioning memory and cognition-encoding neurons,” explains André Fenton, a professor in New York University’s Center for Neural Science and the senior author of the paper. “But despite being individually normal, these neurons are abnormal in their interactions, which results in cognitive impairments.
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