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• W2034248731 startingPage "1130" @default.
• W2034248731 abstract "Autism Spectrum Disorders encompass severe developmental disorders characterized by variable degrees of impairment in language, communication and social skills, as well as by repetitive and stereotypic patterns of behaviour. Substantial percentages of autistic patients display peripheral markers of mitochondrial energy metabolism dysfunction, such as (a) elevated lactate, pyruvate, and alanine levels in blood, urine and/or cerebrospinal fluid, (b) serum carnitine deficiency, and/or (c) enhanced oxidative stress. These biochemical abnormalities are accompanied by highly heterogeneous clinical presentations, which generally (but by no means always) encompass neurological and systemic symptoms relatively unusual in idiopathic autistic disorder. In some patients, these abnormalities have been successfully explained by the presence of specific mutations or rearrangements in their mitochondrial or nuclear DNA. However, in the majority of cases, abnormal energy metabolism cannot be immediately linked to specific genetic or genomic defects. Recent evidence from post-mortem studies of autistic brains points toward abnormalities in mitochondrial function as possible downstream consequences of dysreactive immunity and altered calcium (Ca(2+)) signalling." @default.
• W2034248731 created "2016-06-24" @default.
• W2034248731 creator A5069858700 @default.
• W2034248731 creator A5086216827 @default.
• W2034248731 date "2010-06-01" @default.
• W2034248731 modified "2023-09-29" @default.
• W2034248731 title "Mitochondrial dysfunction in autism spectrum disorders: Cause or effect?" @default.
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• W2034248731 doi "https://doi.org/10.1016/j.bbabio.2010.04.018" @default.
• W2034248731 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20441769" @default.
• W2034248731 hasPublicationYear "2010" @default.
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