Alzheimer's disease: the amyloid hypothesis and the Inverse Warburg effect.

Détails

Ressource 1Télécharger: BIB_62F93479F3D1.P001.pdf (2068.15 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_62F93479F3D1
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Alzheimer's disease: the amyloid hypothesis and the Inverse Warburg effect.
Périodique
Frontiers in Physiology
Auteur(s)
Demetrius L.A., Magistretti P.J., Pellerin L.
ISSN
1664-042X (Electronic)
ISSN-L
1664-042X
Statut éditorial
Publié
Date de publication
01/2015
Peer-reviewed
Oui
Volume
5
Pages
522
Langue
anglais
Notes
Publication types: Journal Article Publication Status: epublish
Résumé
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.
Pubmed
Web of science
Open Access
Oui
Création de la notice
05/02/2015 13:28
Dernière modification de la notice
20/08/2019 14:19
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