Amyloid-β (Aβ) has been proposed as a biomarker and a drug target for the therapy of Alzheimer's disease (AD). The neurotoxic entity and relevance of each conformational form of Aβ to AD pathology is still under debate; Aβ oligomers are considered the major killer form of the peptide whereas monomers have been proposed to be involved in physiological process. Here we reviewed some different effects mediated by monomers and oligomers on mechanisms involved in AD pathogenesis such as autophagy and tau aggregation. Data reported in this review demonstrate that Aβ monomers could have a major role in sustaining the pathogenesis of AD and that AD therapy should be focused not only in the removal of oligomers but also of monomers.

The Unexpected Role of Aβ1-42 Monomers in the Pathogenesis of Alzheimer's Disease.

Tamagno E;Guglielmotto M;VASCIAVEO, VALERIA;
2018

Abstract

Amyloid-β (Aβ) has been proposed as a biomarker and a drug target for the therapy of Alzheimer's disease (AD). The neurotoxic entity and relevance of each conformational form of Aβ to AD pathology is still under debate; Aβ oligomers are considered the major killer form of the peptide whereas monomers have been proposed to be involved in physiological process. Here we reviewed some different effects mediated by monomers and oligomers on mechanisms involved in AD pathogenesis such as autophagy and tau aggregation. Data reported in this review demonstrate that Aβ monomers could have a major role in sustaining the pathogenesis of AD and that AD therapy should be focused not only in the removal of oligomers but also of monomers.
JOURNAL OF ALZHEIMER'S DISEASE
62
3
1241
1245
https://content.iospress.com/articles/journal-of-alzheimers-disease/jad170581
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5870015/
Alzheimer’s disease; Aβ monomers; Aβ oligomers; autophagy; tau protein
Tamagno E, Guglielmotto M, Monteleone D, Manassero G, Vasciaveo V, Tabaton M.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2318/1678334
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