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NDDs are a group of illnesses that impact brain development and function and are defined by a wide range of hereditary and clinical characteristics. The numerous factors that determine the clinical presentation of NDDs are discussed in this review, with a focus on gene vulnerability, mutational load, and the two-hit model. Despite the complicated architecture of NDD mutational processes, the numerous proteins implicated tend to converge on common pathways such as synaptic plasticity/function, chromatin remodelers, and the mammalian target of rapamycin (mTOR) pathway. The identification of candidates that could be targeted for therapeutic approaches would ideally result from a complete understanding of the mechanics behind these pathways.
