Author: Pannuzzo, Martina
Description: Despite tremendous worldwide efforts, clinical trials assessing Alzheimer’s disease (AD)-related therapeutics have been relentlessly unsuccessful. Hence, there is an urgent need to challenge old hypotheses with novel paradigms. An emerging concept is that the amyloid-beta (AB) peptide, which was until recently deemed a major player in the cause of AD, may instead modulate synaptic plasticity and protect against excitotoxicity. The link between AB-mediated synaptic plasticity and AB trafficking is central for understanding AD pathogenesis and remains a perplexing relationship. The crossover between AB pathological and physiological roles is subtle and remains controversial. Based on existing literature, as a signaling molecule, AB is proposed to modulate its own turnover and synaptic plasticity through what is currently believed to be the cause of AD: the transient formation of pore-like oligomers. A change of perspective regarding how AB pores exert a protective function will unavoidably revolutionize the entire field of anti-amyloid drug development.
Subject headings: Alzheimer’s disease; Aging; Beta-amyloid pore; Calcium; Cholesterol dyshomeostasis; Endocytic trafficking; Excitotoxicity; Synaptic plasticity
Publication year: 2021
Journal or book title: Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association
Pages: 1-6
Find the full text: https://www.strategian.com/fulltext/Pannuzzo2021.pdf
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Serial number: 3402