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Synaptic changes in the brain of subjects with schizophrenia
Author(s) -
Faludi Gábor,
Mirnics Károly
Publication year - 2011
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2011.02.013
Subject(s) - synaptic pruning , schizophrenia (object oriented programming) , neuroscience , neuroimaging , disease , psychosis , homeostatic plasticity , psychology , synaptic plasticity , synaptic scaling , metaplasticity , biology , psychiatry , medicine , genetics , microglia , inflammation , pathology , receptor , immunology
Clinical, epidemiological, neuroimaging and postmortem data all suggest schizophrenia is a neurodevelopmental disorder, and that synaptic disturbances might play a critical role in developing the disease. In 1982, Feinberg proposed that the schizophrenia might arise as a result of abnormal synaptic pruning. His hypothesis has survived 40 years of accumulated data, and we review the critical findings related to synaptic dysfunction of schizophrenia. While it is clear that synaptic disturbances are integral and important for understanding the pathophysiology of schizophrenia, it has also become obvious that synaptic disturbances cannot be studied and understood as an independent disease hallmark, but only as a part of a complex network of homeostatic events. Development, glial–neural interaction, changes in energy homeostasis, diverse genetic predisposition, neuroimmune processes and environmental influences all can tip the delicate homeostatic balance of the synaptic morphology and connectivity in a uniquely individual fashion, thus contributing to the emergence of the various symptoms of this devastating disorder. Finally, we argue that based on a predominant change in gene expression pattern we can broadly sub‐stratify schizophrenia into “synaptic” “oligodendroglial”, “metabolic” and “inflammatory” subclasses.