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Brain region‐specific deficit in mitochondrial electron transport chain complexes in children with autism
Open accessAbstract
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, 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]
In the citing paper
“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 the citing paper
“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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Cites
Mitochondrial free radical generation, oxidative stress, and aging
Cadenas, E., & Davies, K. J. A. (2000) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(00)00317-8 · Cited by 3,010
Mitochondrial Complex I Deficiency in Parkinson's Disease
Schapira, A. H. V., Cooper, J. M., Dexter, D., Clark, J. B., Jenner, P., & Marsden, C. D. (1990) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1990.tb02325.x · Cited by 2,283
MITOCHONDRIAL COMPLEX I DEFICIENCY IN PARKINSON'S DISEASE
Schapira, A. H. V., Cooper, J. A. D., Dexter, D. T., Jenner, P. G., Clark, J. B., & MARSDEN, C. D. (1989) · The Lancet · doi:10.1016/s0140-6736(89)92366-0 · Cited by 1,757
Histoanatomic observations of the brain in early infantile autism
Bauman, M., & Kemper, T. L. (1985) · Neurology · doi:10.1212/wnl.35.6.866 · Cited by 964
James, S. J., Cutler, P., Melnyk, S., Jernigan, S., Janak, L., Gaylor, D. W., & Neubrander, J. A. (2004) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/80.6.1611 · Cited by 955
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Bauman, M. L., & Kemper, T. L. (2005) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2004.09.006 · Cited by 919
Rice, C. E. (2009) · PsycEXTRA Dataset · doi:10.1037/e562722010-001 · Cited by 762
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Gu, M., Gash, M. T., Mann, V. M., Javoy‐Agid, F., Cooper, J. M., & Schapira, A. H. V. (1996) · Annals of Neurology · doi:10.1002/ana.410390317 · Cited by 758
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Research works printed but not linked: 1
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Additional file 5 of SETD5 haploinsufficiency affects mitochondrial compartment in neural cells
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Additional file 4 of SETD5 haploinsufficiency affects mitochondrial compartment in neural cells
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Additional file 7 of SETD5 haploinsufficiency affects mitochondrial compartment in neural cells
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Additional file 1 of SETD5 haploinsufficiency affects mitochondrial compartment in neural cells
Zaghi, M., Longo, F., Massimino, L., Rubio, A., Bido, S., Mazzara, P. G., Bellini, E. N., Banfi, F., Podini, P., Maltecca, F., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26593220
Additional file 3 of SETD5 haploinsufficiency affects mitochondrial compartment in neural cells
Zaghi, M., Longo, F., Massimino, L., Rubio, A., Bido, S., Mazzara, P. G., Bellini, E. N., Banfi, F., Podini, P., Maltecca, F., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26593226
Additional file 8 of SETD5 haploinsufficiency affects mitochondrial compartment in neural cells
Zaghi, M., Longo, F., Massimino, L., Rubio, A., Bido, S., Mazzara, P. G., Bellini, E. N., Banfi, F., Podini, P., Maltecca, F., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26593241
Additional file 2 of SETD5 haploinsufficiency affects mitochondrial compartment in neural cells
Zaghi, M., Longo, F., Massimino, L., Rubio, A., Bido, S., Mazzara, P. G., Bellini, E. N., Banfi, F., Podini, P., Maltecca, F., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26593223
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Metadata
- 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
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