title: Degeneration of microglial cells in frontal and temporal lobes of chronic schizophrenics.
abstract: Schizophrenia is a social disease that occurs in 0.5-1% of the population. It shows a high variability in both clinical picture and theory of its pathogenesis. Its clinical manifestations are accompanied by biochemical, immunological and structural changes. A pivotal role in the development of psychotic disorders is attributed to the impaired limbic system. The aim of this study was to find out whether, and if so, to what extent immunocompetent cells of the central nervous system (microglia) are involved in the process of degeneration occuring in these structures. The study was carried out on 12 brains of female chronic schizophrenics. Sections of frontal and temporal cortex were subjected to ultrastructural as well as histochemical and immunohistochemical examinations by light microscopy. In the structures under study, a large number of ramified microglial cells showing on their surface the expression of the major histocompatibility complex class II (MHC II) was observed. Most cells showed degenerative traits (cytoplasm shrinkage, thinning, shortening and fragmentation of their processes) up to apoptotic changes. Perivascular microglia displayed the lowest intensity of degenerative changes. Ultrastructurally, some damaged microglial cells contained phagosomes and/or degenerated mitochondria. Most abnormal microglia showed morphological signs of the former normal function of immunocompetent and phagocytosing cells. Degeneration of microgial cells, resulting most likely from the primary impairment of the neuron-glia communication that damages their immunocompetent function, may lead to the exacerbation of structural damage and psychotic symptoms. Treatment of chronic schizophrenics should involve the supply of agents to prevent degeneration of microglia and/or long-term immunotherapy.
authors.affiliation: Department of Neuropathology, Institute of Psychiatry and Neurology, Warszawa, Poland. bobrow@ipin.edu.pl
authors.forename: Teresa
authors.initials: T
authors.lastname: Wierzba-Bobrowicz
authors.forename: Eliza
authors.initials: E
authors.lastname: Lewandowska
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Kosno-Kruszewska
authors.forename: Waldemar
authors.initials: W
authors.lastname: Lechowicz
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Pasennik
authors.forename: Bogna
authors.initials: B
authors.lastname: Schmidt-Sidor
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000502:physiology; D005260:Female; D005625:Frontal Lobe / Q000473:pathology* / Q000648:ultrastructure; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017628:Microglia / Q000378:metabolism* / Q000648:ultrastructure; D008854:Microscopy, Electron; D008875:Middle Aged; D012559:Schizophrenia / Q000473:pathology*; D013702:Temporal Lobe / Q000473:pathology* / Q000648:ultrastructure
chemical_list: D000949:Histocompatibility Antigens Class II