Glutamate and schizophrenia and the n-methyl-d-aspartate receptor hypofunction hypothesis

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Abstract

Schizophrenic psychoses are severe mental disorders over the course of which hallucinations, changed perception, cognitive disturbances, as well as social withdrawal and lack of drive may occur. There is an increased familial incidence of schizophrenia. Whereas the risk of disease is around 1% in the average population, it increases to over 40% in children of two schizophrenic parents (1). In the meantime, numerous family, twin, and adoption studies have demonstrated that genetic factors make a major contribution to the etiology of schizophrenic psychoses (2,3). Despite these genetically related influences on the development of endogenous psychoses, the genesis of this disease has yet to be explained. Thus, although genetic factors appear to have been confirmed for the etiopathogenesis of schizophrenic psychoses, the results of other research work have been all the more heterogeneous over the past years. © 2005 Humana Press.

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Bleich, S., & Kornhuber, J. (2005). Glutamate and schizophrenia and the n-methyl-d-aspartate receptor hypofunction hypothesis. In Dopamine and Glutamate in Psychiatric Disorders (pp. 169–179). Humana Press. https://doi.org/10.1007/978-1-59259-852-6_7

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