Mitochondrial dysfunction in schizophrenia: Pathways, mechanisms and implications.

Rajasekaran, A, Venkatasubramanian, G, Berk, Michael and Debnath, M 2015, Mitochondrial dysfunction in schizophrenia: Pathways, mechanisms and implications., Neuroscience and Biobehavioral Reviews, vol. 48, pp. 10-21, doi: 10.1016/j.neubiorev.2014.11.005.

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Title Mitochondrial dysfunction in schizophrenia: Pathways, mechanisms and implications.
Author(s) Rajasekaran, A
Venkatasubramanian, G
Berk, MichaelORCID iD for Berk, Michael orcid.org/0000-0002-5554-6946
Debnath, M
Journal name Neuroscience and Biobehavioral Reviews
Volume number 48
Start page 10
End page 21
Total pages 12
Publisher Elsevier
Place of publication Amsterdam, The Netherlands
Publication date 2015-01-01
ISSN 1873-7528
Keyword(s) Inflammation
Mitochondria
Neuroprogression
Oxidative stress
Schizophrenia
Science & Technology
Life Sciences & Biomedicine
Behavioral Sciences
Neurosciences
Neurosciences & Neurology
OXIDATIVE STRESS MARKERS
COMPLEX-I ACTIVITY
N-ACETYL CYSTEINE
PROGRESSIVE BRAIN CHANGES
BLOOD MONONUCLEAR-CELLS
BIPOLAR DISORDER
PSYCHOTIC DISORDERS
NITROSATIVE STRESS
CYTOCHROME-C
DOUBLE-BLIND
Summary Mitochondria play a critical role in regulating cellular functions including bioenergetics, calcium homeostasis, redox signalling, and apoptotic cell death. Mitochondria are also essential to many aspects of neurodevelopment and neuronal functions. However, mitochondrial impairment may affect bioenergetics in the developing brain and alter critical neuronal processes leading to neurodevelopmental abnormalities. Schizophrenia is a chronic and severe neuropsychiatric disorder of neurodevelopmental origin. Immuno-inflammatory pathway is one of the widely appreciated mechanisms that has consistently been implicated in the neurodevelopmental origin of schizophrenia. However, the source of inflammation and the underlying neurobiological mechanisms leading to schizophrenia are yet to be fully ascertained. Recent understanding reveals that perturbation of mitochondrial network dynamics might lead to various nervous system disorders with inflammatory pathologies. Mitochondrial deficit, altered redox balance and chronic low-grade inflammation are evident in schizophrenia. It is hypothesized that oxidative/nitrosative stress responses due to mitochondrial dysfunctions might activate immuno-inflammatory pathways and subsequently lead to neuroprogressive changes in schizophrenia. Herein, we summarise the current understanding of molecular links between mitochondrial dysfunctions and pathogenesis of schizophrenia based on evidence from genomics, proteomics and imaging studies, which together support a role for mitochondrial impairment in the pathogenetic pathways of schizophrenia.
Language eng
DOI 10.1016/j.neubiorev.2014.11.005
Field of Research 110319 Psychiatry (incl Psychotherapy)
111714 Mental Health
11 Medical And Health Sciences
17 Psychology And Cognitive Sciences
Socio Economic Objective 920410 Mental Health
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, Elsevier
Persistent URL http://hdl.handle.net/10536/DRO/DU:30068837

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
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