Mitochondrial abnormalities in temporal lobe of autistic brain
Open accessAbstract
Autism spectrum disorder (ASD) consists of a group of complex developmental disabilities characterized by impaired social interactions, deficits in communication and repetitive behavior. Multiple lines of evidence implicate mitochondrial dysfunction in ASD. In postmortem BA21 temporal cortex, a region that exhibits synaptic pathology in ASD, we found that compared to controls, ASD patients exhibited altered protein levels of mitochondria respiratory chain protein complexes, decreased Complex I and IV activities, decreased mitochondrial antioxidant enzyme SOD2, and greater oxidative DNA damage. Mitochondrial membrane mass was higher in ASD brain, as indicated by higher protein levels of mitochondrial membrane proteins Tom20, Tim23 and porin. No differences were observed in either mitochondrial DNA or levels of the mitochondrial gene transcription factor TFAM or cofactor PGC1α, indicating that a mechanism other than alterations in mitochondrial genome or mitochondrial biogenesis underlies these mitochondrial abnormalities. We further identified higher levels of the mitochondrial fission proteins (Fis1 and Drp1) and decreased levels of the fusion proteins (Mfn1, Mfn2 and Opa1) in ASD patients, indicating altered mitochondrial dynamics in ASD brain. Many of these changes were evident in cortical pyramidal neurons, and were observed in ASD children but were less pronounced or absent in adult patients. Together, these findings provide evidence that mitochondrial function and intracellular redox status are compromised in pyramidal neurons in ASD brain and that mitochondrial dysfunction occurs during early childhood when ASD symptoms appear.
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The reduction of mTOR-regulated neuronal autophagy is consistent with recent findings of a lack of autophagic mitochondrial turnover in ASD brains.
“The reduction of mTOR-regulated neuronal autophagy is further consistent with our recent findings of a lack of autophagic mitochondrial turnover in ASD brains (Tang et al., 2013).”
From Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits (2014) · cites this paper as Tang et al., 2013
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- Authors
- Tang, G., Gutierrez Rios, P., Kuo, S.-H., Akman, H. O., Rosoklija, G., Tanji, K., Dwork, A., Schon, E. A., DiMauro, S., Goldman, J., & Sulzer, D.
- Affiliations
- Columbia University (US)
- Columbia University Irving Medical Center (US)
- Corresponding author
- Sulzer, David
- ORCID
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 54
- Pages
- 349-361
- ISSN
- 0969-9961 (ISSN-L)
- PMC
- PMC3959772
- OpenAlex
- W2060836360
- Cited by
- 194
- References
- 79
- Citations by year
- 2026: 13 · 2025: 11 · 2024: 12 · 2023: 18 · 2022: 16 · 2021: 23 · 2020: 23 · 2019: 9 · 2018: 19 · 2017: 13 · 2016: 10 · 2015: 9 · 2014: 14 · 2013: 4
- FWCI
- 6.76
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Mental Health (R01MH064168, K01MH096956)
- National Institute of Neurological Disorders and Stroke (K08NS083738)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P01HD032062)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- autism spectrum disorder, mitochondrial dysfunction, temporal lobe, respiratory chain complexes, manganese superoxide dismutase, oxidative DNA damage, mitochondrial membrane proteins, mitochondrial dynamics, mitochondrial fission, mitochondrial fusion, pyramidal neurons, redox state, childhood autism
- MeSH terms
- Adolescent, Adult, Autistic Disorder, Child, Child, Preschool, Female, Humans, Male, Middle Aged, Mitochondria, Temporal Lobe, Blotting, Western, Oxidative Stress, Electron Transport Chain Complex Proteins, Young Adult
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