作者: Janelle L Cooper
DOI: 10.2165/00002512-200320060-00001
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摘要: Amyloid plaques and neurofibrillary tangles are the neuropathological hallmarks of Alzheimer's disease (AD), but no conclusive evidence has emerged showing that these cause not a product disease. Many studies have implicated oxidation inflammation in AD process, there is growing abnormalities lipid metabolism also play role. Using epidemiology to elucidate risk factors histological changes suggest possible mechanisms, hypothesis advanced dietary lipids principal factor for development late-onset sporadic AD. The degree saturation fatty acids position first double bond essential most critical determining effect fats on AD, with unsaturated n-3 bonds conferring protection an overabundance saturated or n-6 increasing risk. interaction apolipoprotein E isoforms may determine rate sustained autoperoxidation within cellular membranes efficacy membrane repair. Interventions involving show great promise slowing possibly averting including changes, cholesterol-modifying agents antioxidants.