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• W2019453676 abstract "Epidemiological and biochemical studies show that the sporadic forms of Alzheimer’s disease (AD) are characterized by the following hallmarks : (a) An exponential increase with age ; (b) Selective neuronal vulnerability ; (c) Inverse cancer comorbidity. The present article appeals to these hallmarks to evaluate and contrast two competing models of AD : the amyloid hypothesis (a neuron-centric mechanism) and the Inverse Warburg hypothesis (a neuron-astrocytic mechanism). We show that these three hallmarks of AD conflict with the amyloid hypothesis, but are consistent with the Inverse Warburg hypothesis, a bioenergetic model which postulates that AD is the result of a cascade of three events – mitochondrial dysregulation, metabolic reprogramming (the Inverse Warburg effect), and natural selection. We also provide an explanation for the failures of the clinical trials based on amyloid immunization, and we propose a new class of therapeutic strategies consistent with the neuroenergetic selection model." @default.
• W2019453676 created "2016-06-24" @default.
• W2019453676 creator A5015544182 @default.
• W2019453676 creator A5037451153 @default.
• W2019453676 creator A5045897447 @default.
• W2019453676 date "2015-01-14" @default.
• W2019453676 modified "2023-10-06" @default.
• W2019453676 title "Alzheimer's disease: the amyloid hypothesis and the Inverse Warburg effect" @default.
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• W2019453676 doi "https://doi.org/10.3389/fphys.2014.00522" @default.
• W2019453676 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4294122" @default.
• W2019453676 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25642192" @default.
• W2019453676 hasPublicationYear "2015" @default.
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