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A. Poduri, G. Evrony, X. Cai and C. A. Walsh, “Somatic Mutation, Genomic Variation, and Neurological Disease,” Science, Vol. 341, No. 6141, 2013, Article ID: 1237758.

has been cited by the following article:

• TITLE: Pathophysiology of Schizophrenia Based on Impaired Glial-Neuronal Interactions

  AUTHORS: Bernhard J. Mitterauer

  KEYWORDS: Schizophrenia; Glial-Neuronal Interactions; Impairments

  JOURNAL NAME: Open Journal of Medical Psychology, Vol.3 No.2, January 17, 2014

  ABSTRACT: The model of impaired glial-neuronal interactions in schizophrenia is based on the core hypothesis that non-functional astrocyte receptors may cause an unconstrained synaptic information flux such that glia lose their modulatory function in tripartite synapses. This may lead to a generalization of information processing in the neuronal networks responsible for delusions and hallucinations on the behavioral level. In this acute paranoid stage of schizophrenia, non-functional astrocytic receptors or their loss decompose the astrocyte domain organization with the effect that a gap between the neuronal and the glial networks arises. If the illness progresses the permanent synaptic neurotransmitter flux may additionally impair the oligodendrocyte-axonic interactions, accompanied by a “creeping” decay of oligodendroglia, axons and glial gap junctions responsible for severe cognitive impairment. Here we may deal with after-effects caused by the basic fault of information processing in tripartite synapses. The gaps between the neuronal and glial networks prohibit the neuronal reality testing of intentional programs presumably generated in the glial networks, called schizophrenic dysintentionality. In non-schizophrenic delusions glia may not be disturbed, but exhausted extrasynaptic information processing may cause an unconstrained synaptic flux responsible for delusions.