Association between amyloid-β (Aβ) toxicity, mitochondrial dysfunction, oxidative stress
and neuronal damage has been demonstrated in the pathophysiology of Alzheimer's disease (AD). In
the early stages of the disease, the defect in energy metabolism was found to be severe. This may
probably due to the Aβ and ROS-induced declined activity of complexes in electron transport chain
(ETC) as well as damages to mitochondrial DNA. Though clinically inconclusive, supplementation
with antioxidants is reported to be beneficial especially in the early stages of the disease. A mild to
moderate improvement in dementia is possible with therapy using antioxidants viz coenzyme Q10
(ubiquinone), α-lipoic acid, selenium, omega-3 fatty acids and vitamin E, emphasize their possible role as an adjuvant
with the existing conventional treatment. Since mitochondrial dysfunction has been observed, a new therapeutic strategy
called as 'Mitochondrial Medicine' which is aimed to maintain the energy production as well as to ameliorate the enhanced
apoptosis of nerve cells, has been developed. Mitochondrial CoQ10, Szeto-Schiller peptide-31 and superoxide dismutase/
catalase mimetic, EUK-207 were the mitochondrial targeted agents demonstrated in experimental studies. This article
discusses the mitochondrial impairment and the possible mitochondria targeted therapeutic intervention in AD.
Keywords: Antioxidants, β-amyloid peptide, electron transport chain, mitochondria, mitochondrial CoQ10, neurodegenerative
diseases, superoxide dismutase/catalase mimetic, Szeto-Schiller peptide-31.
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