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• W2014704142 endingPage "288" @default.
• W2014704142 startingPage "282" @default.
• W2014704142 abstract "According to the amyloid cascade hypothesis, accumulation of the amyloid peptide Aβ, derived by proteolytic processing from the amyloid precursor protein (APP), is the key pathogenic trigger in Alzheimer's disease (AD). This view has led researchers for more than two decades and continues to be the most influential model of neurodegeneration. Nevertheless, close scrutiny of the current evidence does not support a central pathogenic role for Aβ in late-onset AD. Furthermore, the amyloid cascade hypothesis lacks a theoretical foundation from which the physiological generation of Aβ can be understood, and therapeutic approaches based on its premises have failed. We present an alternative model of neurodegeneration, in which sustained cholesterol-associated neuronal distress is the most likely pathogenic trigger in late-onset AD, directly causing oxidative stress, inflammation and tau hyperphosphorylation. In this scenario, Aβ generation is part of an APP-driven adaptive response to the initial cholesterol distress, and its accumulation is neither central to, nor a requirement for, the initiation of the disease. Our model provides a theoretical framework that places APP as a regulator of cholesterol homeostasis, accounts for the generation of Aβ in both healthy and demented brains, and provides suitable targets for therapeutic intervention." @default.
• W2014704142 created "2016-06-24" @default.
• W2014704142 creator A5000250440 @default.
• W2014704142 creator A5087407753 @default.
• W2014704142 date "2013-01-01" @default.
• W2014704142 modified "2023-10-16" @default.
• W2014704142 title "Rational heterodoxy: Cholesterol reformation of the amyloid doctrine" @default.
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