Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41380-021-01249-0
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dc.titleThe Amyloid-beta Pathway in Alzheimer's Disease
dc.contributor.authorHampel, Harald
dc.contributor.authorHardy, John
dc.contributor.authorBlennow, Kaj
dc.contributor.authorChen, Christopher
dc.contributor.authorPerry, George
dc.contributor.authorKim, Seung Hyun
dc.contributor.authorVillemagne, Victor L
dc.contributor.authorAisen, Paul
dc.contributor.authorVendruscolo, Michele
dc.contributor.authorIwatsubo, Takeshi
dc.contributor.authorMasters, Colin L
dc.contributor.authorCho, Min
dc.contributor.authorLannfelt, Lars
dc.contributor.authorCummings, Jeffrey L
dc.contributor.authorVergallo, Andrea
dc.date.accessioned2022-04-08T07:11:59Z
dc.date.available2022-04-08T07:11:59Z
dc.date.issued2021-08-30
dc.identifier.citationHampel, 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
dc.identifier.issn1359-4184
dc.identifier.issn1476-5578
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/218739
dc.description.abstractBreakthroughs 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.
dc.language.isoen
dc.publisherSPRINGERNATURE
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectBiochemistry & Molecular Biology
dc.subjectNeurosciences
dc.subjectPsychiatry
dc.subjectNeurosciences & Neurology
dc.subjectBASAL FOREBRAIN ATROPHY
dc.subjectAPOLIPOPROTEIN-E GENOTYPE
dc.subjectBLOOD-BRAIN-BARRIER
dc.subjectDENSITY-LIPOPROTEIN RECEPTOR
dc.subjectIMPAIR SYNAPTIC PLASTICITY
dc.subjectGAMMA-SECRETASE ACTIVITY
dc.subjectGENOME-WIDE ASSOCIATION
dc.subjectPRECURSOR PROTEIN GENE
dc.subjectA-BETA
dc.subjectCEREBROSPINAL-FLUID
dc.typeReview
dc.date.updated2022-04-08T02:34:10Z
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1038/s41380-021-01249-0
dc.description.sourcetitleMOLECULAR PSYCHIATRY
dc.description.volume26
dc.description.issue10
dc.description.page5481-5503
dc.published.statePublished
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