Skewed signaling in striatum may spawn repetitive behaviors
Synaptic changes in the brain region could drive a core trait of fragile X syndrome, a new mouse study suggests.
Synaptic changes in the brain region could drive a core trait of fragile X syndrome, a new mouse study suggests.
A protective pathway that pauses protein synthesis is muted in a mouse model of fragile X syndrome, according to a new study.
Contrary to conventional wisdom, most people with fragile X syndrome express the FMR1 gene — albeit improperly.
The approach prompts cultured cells to correct the genetic mutation in fragile X syndrome using their own DNA repair system, but it still needs to be tested further.
A shift in astrocyte secretions may explain the atypical firing patterns of neurons derived from people with fragile X syndrome.
The phase 2A trial has its detractors despite positive animal results and is being sponsored by a company that is struggling financially.
This month’s newsletter takes a close look at the orphan drug program in the United States, several cannabis-based therapies and a secondary analysis of bumetanide, among other new developments in autism-related drug trials.
FMR1 loss impairs sodium channels, hindering mouse neurons from generating the electrical signals needed to transmit information.
Cells from people with fragile X syndrome overproduce — but don’t accumulate — proteins. New work suggests that excessive protein breakdown may account for this discrepancy, and explain some of the syndrome’s traits.
The circuit linking the prefrontal cortex and part of the thalamus is impaired in mice raised in social isolation and in mice with mutations in the FMR1 or TSC2 genes.