Abstract
BackgroundMitochondrial dysfunction and defects in oxidative metabolism are a characteristic feature of many chronic illnesses not currently classified as mitochondrial diseases. Examples of such illnesses include bipolar disorder, multiple sclerosis, Parkinson’s disease, schizophrenia, depression, autism, and chronic fatigue syndrome.DiscussionWhile the majority of patients with multiple sclerosis appear to have widespread mitochondrial dysfunction and impaired ATP production, the findings in patients diagnosed with Parkinson’s disease, autism, depression, bipolar disorder schizophrenia and chronic fatigue syndrome are less consistent, likely reflecting the fact that these diagnoses do not represent a disease with a unitary pathogenesis and pathophysiology. However, investigations have revealed the presence of chronic oxidative stress to be an almost invariant finding in study cohorts of patients afforded each diagnosis. This state is characterized by elevated reactive oxygen and nitrogen species and/or reduced levels of glutathione, and goes hand in hand with chronic systemic inflammation with elevated levels of pro-inflammatory cytokines.SummaryThis paper details mechanisms by which elevated levels of reactive oxygen and nitrogen species together with elevated pro-inflammatory cytokines could conspire to pave a major road to the development of mitochondrial dysfunction and impaired oxidative metabolism seen in many patients diagnosed with these disorders.
Highlights
Mitochondrial dysfunction and defects in oxidative metabolism are a characteristic feature of many chronic illnesses not currently classified as mitochondrial diseases
Summary This paper has detailed some of the evidence demonstrating the existence of immune dysfunction, oxidative stress, and mitochondrial dysfunction in many patients diagnosed with multiple sclerosis (MS), Parkinson’s disease (PD), autism, bipolar disorder, depression, schizophrenia, and chronic fatigue syndrome (CFS)
nitric oxide (NO), and Pro-inflammatory cytokine (PIC) clearly have the capacity to inhibit the activity of the electron transport chain (ETC) at several points, alone or synergistically, leading to the depletion of adenosine triphosphate (ATP) production and promoting a switch to anaerobic glycolysis
Summary
Mitochondrial dysfunction and defects in oxidative metabolism are a characteristic feature of many chronic illnesses not currently classified as mitochondrial diseases. Mitochondrial dysfunction with concomitant oxidative stress is evidenced in the brains and periphery of many patients with the diagnoses of multiple sclerosis (MS) [6], chronic fatigue syndrome (CFS) [6], Parkinson’s disease (PD) [7], and autism [8]. Mitochondrial dysfunction in such individuals may well result from the presence of oxidative stress, as there is ample evidence implicating oxidative stress as one of the major contributing factors in the development of mitochondrial dysfunction and compromised bioenergetic performance [9,10,11,12,13]. These reactive species can be generated by activated inflammatory cells, including
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