The most common inherited cause of mental retardation, fragile X syndrome owes its name and symptoms to a mutation on the X chromosome, causing the loss of a key regulatory protein known as fragile X mental retardation protein (FMRP). Clinical trials for drugs targeting the impacts of this defect on neurons raised hopes of a breakthrough, but the results were disappointing. New research suggests the answer might be found in glial cells, supporting cells in the brain, and especially in astrocytes, in which FMRP (highlighted in green in this cell) is normally found. In mice, losing FMRP in astrocytes affected synapse formation between neurons, a symptom also seen in fragile X patients. As humans have far more astrocytes than other animals, these cells may have an even greater role to play, suggesting that defects in both neurons and glial cells must be addressed in order to treat fragile X.
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