PerspectiveNEURODEVELOPMENT

“RASopathic” astrocytes constrain neural plasticity

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Science  08 May 2015:
Vol. 348, Issue 6235, pp. 636-637
DOI: 10.1126/science.aab3738

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Summary

Over the past decade, mutations in genes encoding RAS family members, other components of an intracellular signaling cascade that RAS controls, and proteins that modify the cascade have been recognized as causes of developmental syndromes. Collectively, these syndromes are often referred to as “RASopathies.” Not surprisingly, RASopathies have numerous manifestations, including propensity to cancer, craniofacial abnormalities, cardiac defects, cutaneous abnormalities, neurodevelopmental delay, and varying degrees of cognitive dysfunction. Uncovering the causes and developing treatments for the neurodevelopmental abnormalities are a challenge because of the myriad cellular elements in the brain and the complexity of nervous system function. A recent study by Krencik et al. (1) takes a major step toward identifying the cellular pathology underlying Costello syndrome, a RASopathy that is characterized by delayed development, craniofacial and heart problems, and cognitive impairment. The latter appears to be linked to abnormal development and function of a population of nonneuronal cells (astrocytes) in the brain.