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BMC Med. 2015 Apr 1;13:68. doi: 10.1186/s12916-015-0310-y.

The many roads to mitochondrial dysfunction in neuroimmune and neuropsychiatric disorders.

Morris G1, Berk M2,3,4,5.

Author information

1
Tir Na Nog, Bryn Road seaside 87, Llanelli, Cardiff, Wales, SA152LW, UK. activatedmicroglia@gmail.com.
2
IMPACT Strategic Research Centre, School of Medicine, Deakin University, PO Box 291, Geelong, 3220, Australia. mikebe@barwonhealth.org.au.
3
Orygen Youth Health Research Centre and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052, Australia. mikebe@barwonhealth.org.au.
4
The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052, Australia. mikebe@barwonhealth.org.au.
5
Department of Psychiatry, University of Melbourne, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia. mikebe@barwonhealth.org.au.

Abstract

BACKGROUND:

Mitochondrial dysfunction and defects in oxidative metabolism are a characteristic feature of many chronic illnesses not currently classified as mitochondrial diseases. Examples of such illnesses include bipolar disorder, multiple sclerosis, Parkinson's disease, schizophrenia, depression, autism, and chronic fatigue syndrome.

DISCUSSION:

While the majority of patients with multiple sclerosis appear to have widespread mitochondrial dysfunction and impaired ATP production, the findings in patients diagnosed with Parkinson's disease, autism, depression, bipolar disorder schizophrenia and chronic fatigue syndrome are less consistent, likely reflecting the fact that these diagnoses do not represent a disease with a unitary pathogenesis and pathophysiology. However, investigations have revealed the presence of chronic oxidative stress to be an almost invariant finding in study cohorts of patients afforded each diagnosis. This state is characterized by elevated reactive oxygen and nitrogen species and/or reduced levels of glutathione, and goes hand in hand with chronic systemic inflammation with elevated levels of pro-inflammatory cytokines.

SUMMARY:

This paper details mechanisms by which elevated levels of reactive oxygen and nitrogen species together with elevated pro-inflammatory cytokines could conspire to pave a major road to the development of mitochondrial dysfunction and impaired oxidative metabolism seen in many patients diagnosed with these disorders.

PMID:
25889215
PMCID:
PMC4382850
DOI:
10.1186/s12916-015-0310-y
[Indexed for MEDLINE]
Free PMC Article

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