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I was reading some new information that is being passed around in other neuro sites. There is a new link between mitochondrial dysfunction and autism. So I just wanted to see what the research was on mitochondrial dysfunction and seizures. I have learned that many with autism also have a seizure disorder. I have one child with each, so it is of interest to me.
I will be following this very closely.
I will be following this very closely.
https://www.novapublishers.com/catalog/product_info.php?products_id=1426Mitochondrial Dysfunction And Oxidative Stress In Epilepsy (pp. 105-137)
Authors: Cock, Hannah R. (St Georges Hospital Medical School, London, UK)
Mitochondria, in addition to a primary role in energy production, are of increasingly recognized importance in intracellular calcium homeostasis, signalling and ROS (reactive oxygen species or free radicals) production. The role of mitochondria in excitotoxic cell death in many disease states has been extensively studied, and in recent years this has extended to studies of mitochondrial function in seizure related cell death. The process of mitochondrial permeability transition, releasing chemicals into the cytoplasm that initiate cell death pathways, is central in this context. Numerous triggers to permeability transition have now been identified. Many, if not all may act specifically through effects on the redox state of the cell and oxidative stress. There is accumulating evidence that seizures disrupt normal redox homeostasis in the cell. This may be important for seizure related cell death, and have significant functional consequences in surviving neurons. However, which of these changes are compensatory following seizures, and which might be involved both in epileptogenesis and/or neurological damage as a result of seizures requires further study. In addition, many factors including genetic background, seizure type and duration may influence to what extent the biochemical consequences of seizures are detrimental. Reliable markers of pathological, as opposed to physiological, changes are required, which then need to be validated in a clinical setting. This is particularly so given the emerging evidence supporting a role for Reactive oxygen species (ROS or free radicals) in physiological intracellular signalling. At present a range of antioxidant and other neuroprotective strategies appear promising in principle, but detailed studies across a range of in vivo seizure models, in clinically relevant paradigms, are needed before human trials should be considered.
http://www.ncbi.nlm.nih.gov/pubmed/15544915Mitochondrial dysfunction and oxidative stress: cause and consequence of epileptic seizures.
Department of Pharmaceutical Sciences, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262, USA. firstname.lastname@example.org
Mitochondrial dysfunction has been implicated as a contributing factor in diverse acute and chronic neurological disorders. However, its role in the epilepsies has only recently emerged. Animal studies show that epileptic seizures result in free radical production and oxidative damage to cellular proteins, lipids, and DNA. Mitochondria contribute to the majority of seizure-induced free radical production. Seizure-induced mitochondrial superoxide production, consequent inactivation of susceptible iron-sulfur enzymes, e.g., aconitase, and resultant iron-mediated toxicity may mediate seizure-induced neuronal death. Epileptic seizures are a common feature of mitochondrial dysfunction associated with mitochondrial encephalopathies. Recent work suggests that chronic mitochondrial oxidative stress and resultant dysfunction can render the brain more susceptible to epileptic seizures. This review focuses on the emerging role of oxidative stress and mitochondrial dysfunction both as a consequence and as a cause of epileptic seizures.
PMID: 15544915 [PubMed - indexed for MEDLINE]
http://www.huffingtonpost.com/david-kirby/the-next-big-autism-bomb_b_93627.htmlOn Tuesday, March 11, a conference call was held between vaccine safety officials at the US Centers for Disease Control and Prevention, several leading experts in vaccine safety research, and executives from America's Health Insurance Plans, (the HMO trade association) to discuss childhood mitochondrial dysfunction and its potential link to autism and vaccines.