Often, the best way to
reduce mitochondrial dysfunction is to take preventative steps to reduce exposure to free radicals, which may cause further damage to the mitochondria.
Not exact matches
In cell culture, low concentrations of these corrector molecules can
reduce mitochondrial impairment and neuronal
dysfunction.
Other potential strategies for limiting oxidative stress in neurodegenerative diseases include
reducing the production of nitric oxide, or preventing
mitochondrial dysfunction.
Enhanced amyloidogenic processing of APP by the ß - site APP cleaving enzyme (BACE) and the γ - secretase complex and
reduced clearance lead to increased intracellular levels of soluble oligomeric Aß, resulting in cellular
dysfunction comprising e.g., synaptic failure,
mitochondrial dysfunction, enhanced oxidative stress, neurotransmitter and neurotrophin depletion, inflammation, and apoptosis which is reflected in patients as clinical symptoms such as cognitive deficits [2, 3].
Mitochondrial dysfunction in lupus patients is associated with
reduced glutathione and SOD (superoxide dismutase) levels as well as abnormal energy production.
Treatment for
mitochondrial dysfunction can
reduce your risk of developing the above health conditions, as well as deliver a natural increase to your energy level and improve your overall sense of well - being.
In many situations,
reducing exposure to free radicals and increasing antioxidant consumption can protect the mitochondria and offer some relief from
mitochondrial dysfunction.
High Vitamin C supplementation
reduces amyloid plaque deposition (cause of AD), blood brain barrier disruptions and
mitochondrial dysfunction in the brains.
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).