Cognitive processes require gamma-amino-butyric acid (GABA) interneurons. Via complex synaptic connections, these cells regulate cellular excitability and synaptic plasticity of principal neurons, balancing the excitatory/inhibitory (E/I) tone in cortical networks. Loss of and impairment in function of parvalbumin (PV) interneurons and GABAergic synapses is associated with cognitive impairment in schizophrenia and other psychiatric disorders. Despite efforts to identify the molecular factors leading to E/I imbalance and impaired PV interneuron functioning, much remains to be learned.

Genetically inherited mutations in the fibroblast growth factor 14 (FGF14) gene lead to spinocerebellar ataxia type 27 (SCA27), an autosomal dominant disorder characterized by heterogeneous motor and cognitive impairments. Consistently, genetic deletion of Fgf14 in Fgf14−/− mice recapitulates salient features of the SCA27 human disease.