Glutamate receptors, microtubule associated proteins and developmental anomaly in schizophrenia: An hypothesis

Abstract

In recent years much emphasis has been placed on pathological changes in the medial temporal lobe in schizophrenia along with a possible developmental explanation for this. These separate facts give hope to the notion that it may be possible to formulate a mechanism at the biochemical level to explain how a failure of development may bring about these changes, thereby ushering in an era of mechanistic neurochemical research which has been so fruitful to the understanding of pathology in, for example, Alzheimer's disease and Parkinson's disease. The aim of this editorial is to postulate a hypothesis which links developmental abnormalities in intracellular cytoskeletal assembly with pathological and neurotransmitter abnormalities known to occur in schizophrenia. The hypothesis will state that developmental abnormalities seen in the temporal lobe are due to faulty assembly of microtubule associated proteins due to a deficiency of trophic forms of non-N-methyl-D-aspartate (NMDA) receptors, and that the pathological and neurochemical abnormalities seen in the adult temporal lobe in schizophrenia give evidence for this hypothesis. © 1993, Cambridge University Press. All rights reserved.