Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common type of dementia in elderly ( >65years of age). Excessive extra cellular deposits of amyloid beta (Aβ) are a pathological feature of AD. Aβ can cause cell death through oxidative damage; recent studies have implicated opening of mPTP as a detrimental event in AD-related mitochondrial dysfunctions. Over the past few years, natural compounds with antioxidant properties have shown promise for intervention in AD.
Copyright © 2017 Elsevier B.V. All rights reserved.
MeSH terms
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Amyloid beta-Peptides / pharmacology*
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Apoptosis / drug effects
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Cell Line, Tumor
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Cell Survival / drug effects
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Cytochromes c / metabolism
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DNA Fragmentation / drug effects
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Drug Synergism
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Humans
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Ion Channel Gating / drug effects
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Membrane Potential, Mitochondrial / drug effects
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Mitochondria / drug effects*
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Mitochondria / metabolism*
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Mitochondrial Membrane Transport Proteins / metabolism
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Mitochondrial Permeability Transition Pore
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Monoterpenes / pharmacology*
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Reactive Oxygen Species / metabolism
Substances
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Amyloid beta-Peptides
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Mitochondrial Membrane Transport Proteins
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Mitochondrial Permeability Transition Pore
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Monoterpenes
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Reactive Oxygen Species
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perillyl alcohol
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Cytochromes c