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Mitochondria and Autism


Senior Member
Found this older forum entry on autismweb.com from 2007


"A final component to the collaboration involves a magnetic resonance spectroscopy (MRS) study with Beatrice Golomb, M.D., Ph.D. of UCSD, which is allowing researchers to look at metabolism directly in the brain using methods that combine with more traditional MRI. This method has allowed Dr. Golomb and her team to relate brain structure directly to metabolic function, both at rest and after exercise designed to tax the leg muscles. The idea is that if someone has an energetics deficit, any extra demand for metabolic resources will pull them away from where they are currently being utilized, such as in the brain."
and this

"To do this, scientists in the research network are relating more classical measures, like blood and muscle biopsy, to new ways of examining metabolites. This work makes use of incredible new technologies, including micro-organic breath analysis and a laser technology to analyze mitochondria in the skin."

I thought that some of the new testing methods they mention are interesting.


Senior Member
"The idea is that if someone has an energetics deficit, any extra demand for metabolic resources will pull them away from where they are currently being utilized, such as in the brain."

that makes a lot of sense, brain would be amongst the lowest priority organs in the body, ie the first to be put on 'low maintenance' if energy required elsewhere


Senior Member
Mitochondrial dysfunction in Autism Spectrum Disorders: cause or effect?

Palmieri L, Persico AM.

Laboratory of Biochemistry and Molecular Biology, Department of Pharmaco-Biology, University of Bari, Via Orabona 4, 70125, Bari, Italy; Consiglio Nazionale delle Ricerche, Institute of Biomembranes and Bioenergetics, Bari, Italy.
Biochim Biophys Acta. 2010 May 1. [Epub ahead of print]

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.

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calcium in:
Endocrine disrupting polyhalogenated organic pollutants interfere with thyroid hormone signalling in the developing brain
The Cerebellum 2008, 26–37


While the dioxin-like PCBs are considered the
most dangerous in terms of general toxicity, this is
not consequently so in relation to neurotoxicity,
where ortho-substituted PCBs are frequently shown
to be more potent (16,17). One of the major
explanations for this divergence seems to be that
ortho-substituted PCBs are more potent in disrupting
Ca2+ homeostasis and Ca2+ signalling pathways
in the central nervous system as shown by in vivo
treatment as well as in vitro studies on neurons such
as cerebellar granule cells (16,18–19). The observed
changes in the levels of the neurotransmitter
dopamine in brain and in neuronal cell cultures
(17,20–21) may be one of the results of this
interference with Ca2+.