Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41380-021-01249-0
Title: The Amyloid-beta Pathway in Alzheimer's Disease
Authors: Hampel, Harald
Hardy, John
Blennow, Kaj
Chen, Christopher 
Perry, George
Kim, Seung Hyun
Villemagne, Victor L
Aisen, Paul
Vendruscolo, Michele
Iwatsubo, Takeshi
Masters, Colin L
Cho, Min
Lannfelt, Lars
Cummings, Jeffrey L
Vergallo, Andrea
Keywords: Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
Neurosciences
Psychiatry
Neurosciences & Neurology
BASAL FOREBRAIN ATROPHY
APOLIPOPROTEIN-E GENOTYPE
BLOOD-BRAIN-BARRIER
DENSITY-LIPOPROTEIN RECEPTOR
IMPAIR SYNAPTIC PLASTICITY
GAMMA-SECRETASE ACTIVITY
GENOME-WIDE ASSOCIATION
PRECURSOR PROTEIN GENE
A-BETA
CEREBROSPINAL-FLUID
Issue Date: 30-Aug-2021
Publisher: SPRINGERNATURE
Citation: Hampel, Harald, Hardy, John, Blennow, Kaj, Chen, Christopher, Perry, George, Kim, Seung Hyun, Villemagne, Victor L, Aisen, Paul, Vendruscolo, Michele, Iwatsubo, Takeshi, Masters, Colin L, Cho, Min, Lannfelt, Lars, Cummings, Jeffrey L, Vergallo, Andrea (2021-08-30). The Amyloid-beta Pathway in Alzheimer's Disease. MOLECULAR PSYCHIATRY 26 (10) : 5481-5503. ScholarBank@NUS Repository. https://doi.org/10.1038/s41380-021-01249-0
Abstract: Breakthroughs in molecular medicine have positioned the amyloid-β (Aβ) pathway at the center of Alzheimer’s disease (AD) pathophysiology. While the detailed molecular mechanisms of the pathway and the spatial-temporal dynamics leading to synaptic failure, neurodegeneration, and clinical onset are still under intense investigation, the established biochemical alterations of the Aβ cycle remain the core biological hallmark of AD and are promising targets for the development of disease-modifying therapies. Here, we systematically review and update the vast state-of-the-art literature of Aβ science with evidence from basic research studies to human genetic and multi-modal biomarker investigations, which supports a crucial role of Aβ pathway dyshomeostasis in AD pathophysiological dynamics. We discuss the evidence highlighting a differentiated interaction of distinct Aβ species with other AD-related biological mechanisms, such as tau-mediated, neuroimmune and inflammatory changes, as well as a neurochemical imbalance. Through the lens of the latest development of multimodal in vivo biomarkers of AD, this cross-disciplinary review examines the compelling hypothesis- and data-driven rationale for Aβ-targeting therapeutic strategies in development for the early treatment of AD.
Source Title: MOLECULAR PSYCHIATRY
URI: https://scholarbank.nus.edu.sg/handle/10635/218739
ISSN: 1359-4184
1476-5578
DOI: 10.1038/s41380-021-01249-0
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