Brain region‐specific deficit in mitochondrial electron transport chain complexes in children with autism
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J. Neurochem. (2011) 117, 209–220. Mitochondria play important roles in generation of free radicals, ATP formation, and in apoptosis. We studied the levels of mitochondrial electron transport chain (ETC) complexes, that is, complexes I, II, III, IV, and V, in brain tissue samples from the cerebellum and the frontal, parietal, occipital, and temporal cortices of subjects with autism and age‐matched control subjects. The subjects were divided into two groups according to their ages: Group A (children, ages 4–10 years) and Group B (adults, ages 14–39 years). In Group A, we observed significantly lower levels of complexes III and V in the cerebellum (p < 0.05), of complex I in the frontal cortex (p < 0.05), and of complexes II (p < 0.01), III (p < 0.01), and V (p < 0.05) in the temporal cortex of children with autism as compared to age‐matched control subjects, while none of the five ETC complexes was affected in the parietal and occipital cortices in subjects with autism. In the cerebellum and temporal cortex, no overlap was observed in the levels of these ETC complexes between subjects with autism and control subjects. In the frontal cortex of Group A, a lower level of ETC complexes was observed in a subset of autism cases, that is, 60% (3/5) for complexes I, II, and V, and 40% (2/5) for complexes III and IV. A striking observation was that the levels of ETC complexes were similar in adult subjects with autism and control subjects (Group B). A significant increase in the levels of lipid hydroperoxides, an oxidative stress marker, was also observed in the cerebellum and temporal cortex in the children with autism. These results suggest that the expression of ETC complexes is decreased in the cerebellum and the frontal and temporal regions of the brain in children with autism, which may lead to abnormal energy metabolism and oxidative stress. The deficits observed in the levels of ETC complexes in children with autism may readjust to normal levels by adulthood.
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In the cerebellum of individuals with autism, levels of lipid hydroperoxide, malonyldialdehyde, 8-hydroxy-2'-deoxyguanosine, protein carbonyl, and 3-nitrotyrosine are significantly increased.
“In the cerebellum, the levels of lipid hydroperoxide [103], a product of fatty acid oxidation; of malonyldialdehyde [104], an end-product of lipid peroxidation; of 8-hydroxy-2’-deoxyguanosine (8-OH-dG) [105, 106], a marker of oxidative DNA damage; of protein carbonyl [107], a marker of protein oxidation; and of 3-nitrotyrosine [108], a marker of protein nitration, were significantly increased in”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [103]
Oxidative stress differentially affects selective brain regions in autism: increased oxidative stress and mitochondrial abnormalities were observed in cerebellum, temporal cortex, and frontal cortex, but not in parietal and occipital cortices.
“Our studies of different brain regions showed that oxidative stress differentially affects selective brain regions, i.e., cerebellum, temporal and frontal cortices, in autism [103–105, 107]. Increased oxidative stress and mitochondrial abnormalities were not observed in the parietal and occipital cortices in autism [103–105, 107].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [103]
In children with autism, there is a brain region-specific deficit in levels of electron transport chain complexes: reduced complexes III and V in the cerebellum, complex I in the frontal cortex, and complexes II, III, and V in the temporal cortex compared to age-matched controls.
“Reduced levels of complexes III and V in the cerebellum, of complex I in the frontal cortex, and of complexes II, III, and V in the temporal cortex were observed in children with autism as compared to age-matched control subjects [103].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [103]
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Altun, H., Şahın, N., Kurutaş, E. B., Karaaslan, U., Sevgen, F. H., & Fındıklı, E. (2018) · Psychiatry and Clinical Psychopharmacology · doi:10.1080/24750573.2018.1470360 · Cited by 36 · see citing works
Kartawy, M., Халиулин, И. Г., & Amal, H. (2021) · Brain Sciences · doi:10.3390/brainsci11060677 · Cited by 36 · see citing works
Role of NAD+, Oxidative Stress, and Tryptophan Metabolism in Autism Spectrum Disorders
Essa, M., Subash, S., Braidy, N., Al-Adawi, S., Lim, C. K., Manivasagam, T., & Guillemin, G. (2013) · International Journal of Tryptophan Research · doi:10.4137/ijtr.s11355 · Cited by 46 · see citing works
Self-citation
- Authors
- Chauhan, A., Gu, F., Essa, M. M., Wegiel, J., Kaur, K., Brown, W. T., & Chauhan, V.
- Affiliations
- New York State Office for People With Developmental Disabilities (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2011-02-24
- Volume
- 117
- Issue
- 2
- Pages
- 209-220
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC4839269
- OpenAlex
- W1577847097
- Cited by
- 243
- References
- 88
- Citations by year
- 2026: 8 · 2025: 14 · 2024: 26 · 2023: 23 · 2022: 19 · 2021: 17 · 2020: 15 · 2019: 6 · 2018: 17 · 2017: 8 · 2016: 11 · 2015: 18 · 2014: 18 · 2013: 19 · 2012: 21
- FWCI
- 9.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense
- Office for People With Developmental Disabilities
- National Institute on Aging (P30AG008051)
- 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, cerebellum, frontal cortex, temporal cortex, oxidative stress, lipid hydroperoxides, brain energy metabolism, children versus adults
- MeSH terms
- Adolescent, Adult, Age Factors, Autistic Disorder, Brain, Child, Child, Preschool, Female, Humans, Lipid Peroxides, Male, Multienzyme Complexes, Postmortem Changes, Case-Control Studies, Reactive Oxygen Species, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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