Open AccessJournal Article
Degeneration of microglial cells in frontal and temporal lobes of chronic schizophrenics.
Teresa Wierzba-Bobrowicz,Eliza Lewandowska,E Kosno-Kruszewska,W Lechowicz,Elżbieta Pasennik,Bogna Schmidt-Sidor +5 more
TLDR
Treatment of chronic schizophrenics should involve the supply of agents to prevent degeneration of microglia and/or long-term immunotherapy, and morphological signs of the former normal function of immunocompetent and phagocytosing cells.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.read more
Citations
More filters
Journal ArticleDOI
Immunological aspects in the neurobiology of suicide : Elevated microglial density in schizophrenia and depression is associated with suicide
Johann Steiner,Hendrik Bielau,Ralf Brisch,Peter Danos,Oliver Ullrich,Christian Mawrin,Hans-Gert Bernstein,Bernhard Bogerts +7 more
TL;DR: In conclusion, immunological factors may play a hitherto underestimated role in suicide, and microglial activation might be interpreted as a consequence of presuicidal stress.
Journal ArticleDOI
Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in Alzheimer's disease.
TL;DR: The role of microglial cells in the pathogenesis of Alzheimer's disease (AD) neurodegeneration is unknown as discussed by the authors, and the role of neuroglial activation occurs in the human brain at sites of neurofibrillary degeneration, however, anti-inflammatory drugs do not prevent or reverse neuronal tau pathology.
Journal ArticleDOI
Microglial senescence: does the brain's immune system have an expiration date?
TL;DR: It is raised the possibility that old age, and perhaps other factors (genetic and epigenetic) adversely affect viability and self-renewal capacity of microglia, resulting in the generation of senescent and/or dysfunctional cells.
Journal ArticleDOI
Microglia in the aging brain.
TL;DR: The concept of microglial senescence is discussed, namely that neurodegeneration could also occur secondary to microglia degeneration, and it is discussed the possibility that structural and phenotypic changes that occur inmicroglia are a direct reflection of the aging process onMicroglia.
Journal ArticleDOI
The immune theory of psychiatric diseases: a key role for activated microglia and circulating monocytes.
Wouter Beumer,Sinead M. Gibney,Roosmarijn C. Drexhage,Lorena Pont-Lezica,Janine Doorduin,Hans C. Klein,Johann Steiner,Thomas J. Connor,Andrew Harkin,Marjan A. Versnel,Hemmo A. Drexhage +10 more
TL;DR: A key role for mononuclear phagocytes in the pathogenesis of major psychiatric disorders is described and it is shown that microglia activation impacts neuronal development and function in brain areas congruent with the altered depressive and schizophrenia‐like behaviors.
References
More filters
Journal ArticleDOI
Implications of normal brain development for the pathogenesis of schizophrenia
TL;DR: The findings suggest that nonspecific histopathology exists in the limbic system, diencephalon, and prefrontal cortex, that the pathology occurs early in development, and that the causative process is inactive long before the diagnosis is made.
Journal ArticleDOI
Decreased dendritic spine density on prefrontal cortical pyramidal neurons in schizophrenia.
Leisa A. Glantz,David A. Lewis +1 more
TL;DR: This region- and disease-specific decrease in dendritic spine density on dorsolateral prefrontal cortex layer 3 pyramidal cells is consistent with the hypothesis that the number of cortical and/or thalamic excitatory inputs to these neurons is altered in subjects with schizophrenia.
Journal ArticleDOI
CXCR4-activated astrocyte glutamate release via TNFalpha: amplification by microglia triggers neurotoxicity.
Paola Bezzi,Maria Domercq,Liliana Brambilla,Rossella Galli,Dominique Schols,Erik De Clercq,Angelo L. Vescovi,Giacinto Bagetta,George Kollias,Jacopo Meldolesi,Andrea Volterra +10 more
TL;DR: It is demonstrated that altered glial communication has direct neuropathological consequences and that agents interfering with CXCR4-dependent astrocyte–microglia signaling prevent neuronal apoptosis induced by the HIV-1 coat glycoprotein, gp120IIIB.
Journal ArticleDOI
A functional neuroanatomy of hallucinations in schizophrenia
David Silbersweig,David Silbersweig,Emily Stern,Emily Stern,Chris D. Frith,C. Cahill,Andrew P. Holmes,S. Grootoonk,J. Seaward,P. McKenna,S. E. Chua,L. Schnorr,Terry Jones,R. S. J. Frackowiak,R. S. J. Frackowiak +14 more
TL;DR: A group study of five patients with classic auditory verbal hallucinations despite medication, demonstrating activations in subcortical nuclei (thalamic, stri-atal), limbic structures (especially hippocampus), and paralimbic regions (parahippocampal and cingulate gyri, as well as orbito-frontal cortex).
Journal ArticleDOI
Inhibition of Microglial Activation Attenuates the Development but not Existing Hypersensitivity in a Rat Model of Neuropathy
TL;DR: It is demonstrated that inhibition of microglial activation attenuated the development of behavioral hypersensitivity in a rat model of neuropathic pain but had no effect on the treatment of existing mechanical allodynia and hyperalgesia.