Besides lipotoxicity (see section V.N) many other molecular mechanisms are involved,
including mitochondrial dysfunction, oxidative stress, intramyocardial inflammation, involvement of the reninangiotensin system, altered insulin signaling or female - specific cardiac glycogen handling as a response to metabolic stress (308), and sex - hormone related myocardial calcium handling (309).
Not exact matches
Mitochondrial diseases
include Leigh syndrome, a progressive and fatal disorder characterized by lesions on the brain that may lead to heart, kidney, vision and breathing complications, and Alpers Disease, a neurologic illness that causes seizures, dementia, spasticity, blindness, liver
dysfunction and cerebral degeneration.
Other potential strategies for limiting oxidative stress in neurodegenerative diseases
include reducing the production of nitric oxide, or preventing
mitochondrial dysfunction.
Lynch says, «I think our results rationalise directed studies toward improving
mitochondrial biogenesis as a long - term therapy in Friedreich's ataxia, and that the goals of therapy must
include not only correcting iron - sulphur enzymes but also other
mitochondrial dysfunction.
Mitochondrial dysfunction is found in several disorders, including Parkinson's disease, cardiovascular disease, and mitochondr
Mitochondrial dysfunction is found in several disorders,
including Parkinson's disease, cardiovascular disease, and
mitochondrialmitochondrial diseases.
Mitochondrial dysfunction plays a role in a host of relatively rare disorders as well as neurodegenerative disorders,
including Parkinson's disease.
Why NAD + Declines during Aging: It's Destroyed This recently published article in cell magazine by David Shultz and David Sinclair reviews several recent studies,
including the June 2016 study by also published in Cell magazine by Camacho - Yeriera and colleagues (CD38 Dictates Age - Related NAD Decline and
Mitochondrial Dysfunction through an SIRT3 - Dependent Mechanism) The study implicates CD38 as a -LSB-...]
It is well documented that impaired glucose metabolism or
mitochondrial dysfunction is one of the major pathological changes observed in various neurodegenerative diseases
including Alzheimer's disease (AD), Parkinson's disease (PD) or Huntington's disease (HD), thus suggesting that regulation of glucose metabolism and maintenance of
mitochondrial homeostasis are critical for brain function.»
A customized dietary protocol, targeted supplementation, and mind - body therapies enabled my dramatic recovery, as did addressing root causes of
dysfunction,
including micronutrient deficiencies, heavy metal toxicity, hypothalamic - pituitary - adrenal axis
dysfunction, sex hormone imbalances, dysbiosis, stealth infections, blood sugar dysregulation, and aberrant
mitochondrial function.
In the small intestine, the effects these drugs have been shown to produce
include inhibition of cyclo - oxygenase,
mitochondrial dysfunction and free radical - induced oxidative changes, all of which contribute to the mucosal damage seen.
This
includes a detailed, yet a fully understandable description of the biochemistry of aerobic respiration versus anaerobic fermentation, glycolysis, the Krebs Cycle, the electron transport chain, lactic acid overproduction and how cancer cells develop as a result of
mitochondrial metabolic
dysfunction leading to genetic errors, resulting in metastasis.
Observed effects
include increased insulin sensitivity, reversal of
mitochondrial dysfunction, reduced stem cell senescence, and extension of lifespan (Bai et al., 2011; Gomes et al., 2013; Yoshino et al., 2011; Zhang et al., 2016).
Dysfunction in energy production, that is,
mitochondrial function impairment, is likely to have a role in the pathogenesis of many neurodegenerative diseases, perhaps
including amyotrophic lateral sclerosis.