Journal
BIOLOGICAL PSYCHIATRY
Volume 83, Issue 9, Pages 722-730Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2017.11.018
Keywords
Alzheimer's disease; Autism; Mitochondria; mtDNA; Nuclear receptors; OXPHOS
Categories
Funding
- Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program [W81XWH-16-1-0400, 0401]
- W.W. Smith Charitable Trust [H1407]
- pilot awards from the Diabetes Research Center at the University of Pennsylvania from National Institutes of Health [DK19525, DK111495]
- National Institutes of Health [MH108592, NS021328, CA182384, OD010944]
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The brain has the highest mitochondrial energy demand of any organ. Therefore, subtle changes in mitochondrial energy production will preferentially affect the brain. Considerable biochemical evidence has accumulated revealing mitochondrial defects associated with neuropsychiatric diseases. Moreover, the mitochondrial genome encompasses over a thousand nuclear DNA genes plus hundreds to thousands of copies of the maternally inherited mitochondrial DNA (mtDNA). Therefore, partial defects in either the nuclear DNA or mtDNA genes or combinations of the two can be sufficient to cause neuropsychiatric disorders. Inherited and acquired mtDNA mutations have recently been associated with autism spectrum disorder, which parallels previous evidence of mtDNA variation in other neurological diseases. Therefore, mitochondrial dysfunction may be central to the etiology of a wide spectrum of neurological diseases. The mitochondria and the nucleus communicate to coordinate energy production and utilization, providing the potential for therapeutics by manipulating nuclear regulation of mitochondrial gene expression.
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