Why animals don’t get schizophrenia and people do

On March 30, 2015 by Joana Rossello

Isn’t this a significant advance in the understanding of schizophrenia as “the price humans paid for language” –as Tim Crow put it in 1997?  In a nutshell, this is how the argument runs in the original paper*. Genes known to be related to schizophrenia sit close to Human Accelerated Regions (HAR), i.e. stretches of genes that have undergone rapid changes since our common ancestor with chimps. In particular, it is shown that HAR-related schizophrenia genes seem to be under a stronger selective pressure than other schizophrenia related genes. Furthermore, among the “culprit” schizophrenia HAR-genes there are those that are in charge of the GABA neurotransmitter in the PFC (prefrontal cortex). Now put these other pieces together: The PFC is, as it were, the sit for high intelligence in Sapiens, GABA controls dopamine which runs uncontrolled in schizophrenia (in PFC in particular) and GABA is critical for speech and language since it is responsible for fast-spiking gamma oscillations at the bottom of the  hierarchy of rhythmic brain oscillations which must synchronize and match the differently hierarchically timed linguistic objects.

Against this background, will schizophrenia be some day conceptualized as a brain arrythmia which disrupts language? Anyway, who would dare to deny that we are closer to the goal of a true convergence among evolutionary theory, genetics and linguistics of schizophrenia (and language and human cognition)?

*Xu, Schadt, Pollard, Roussos & Dudley (2015) Genomic and network patterns of schizophrenia genetic variation in human evolutionary accelerated regions, Molecular biology and evolution, doi: 10.1093/molbev/msv031 




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