Abstract
Amyloid-beta (Aβ) plays a pivotal role in Alzheimer’s disease (AD) pathogenesis, and is the most promising disease-modifying target for AD. A succession of failures in Aβ-targeting clinical trials, however, has prompted questions on whether Aβ is the true cause of AD and a valid therapeutic target. Therefore, current therapeutic targets and intervention strategies must be reconsidered. In addition to Aβ, multiple pathological events such as tau hyperphosphorylation, oxidative stress and neuroinflammation are involved in the disease pathogenesis and cause cross-talk between these pathological pathways, which synergistically drive disease progression. Increasing evidence also reveals that the pathogenesis varies at different stages of the disease. Therefore, targeting Aβ alone at all stages of the disease would not be sufficient to halt or reverse disease progression. In the light of the pathophysiologic similarities between the development of ischemic stroke and AD, we can formulate management strategies for AD from the successful practice of ischemic stroke management, namely the tertiary prevention strategy. These new perspectives of tertiary prevention target both Aβ and different pathological pathways of AD pathogenesis at different stages of the disease, and may represent a promising avenue for the effective prevention and treatment of AD.
Keywords: Alzheimer's disease, beta-amyloid, tau hyperphosphorylation, stroke, therapeutic strategy.
Current Alzheimer Research
Title:Perspectives on the Tertiary Prevention Strategy for Alzheimer’s Disease
Volume: 13 Issue: 3
Author(s): Xian-Le Bu, Shu-Sheng Jiao, Yan Lian and Yan-Jiang Wang
Affiliation:
Keywords: Alzheimer's disease, beta-amyloid, tau hyperphosphorylation, stroke, therapeutic strategy.
Abstract: Amyloid-beta (Aβ) plays a pivotal role in Alzheimer’s disease (AD) pathogenesis, and is the most promising disease-modifying target for AD. A succession of failures in Aβ-targeting clinical trials, however, has prompted questions on whether Aβ is the true cause of AD and a valid therapeutic target. Therefore, current therapeutic targets and intervention strategies must be reconsidered. In addition to Aβ, multiple pathological events such as tau hyperphosphorylation, oxidative stress and neuroinflammation are involved in the disease pathogenesis and cause cross-talk between these pathological pathways, which synergistically drive disease progression. Increasing evidence also reveals that the pathogenesis varies at different stages of the disease. Therefore, targeting Aβ alone at all stages of the disease would not be sufficient to halt or reverse disease progression. In the light of the pathophysiologic similarities between the development of ischemic stroke and AD, we can formulate management strategies for AD from the successful practice of ischemic stroke management, namely the tertiary prevention strategy. These new perspectives of tertiary prevention target both Aβ and different pathological pathways of AD pathogenesis at different stages of the disease, and may represent a promising avenue for the effective prevention and treatment of AD.
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Cite this article as:
Bu Xian-Le, Jiao Shu-Sheng, Lian Yan and Wang Yan-Jiang, Perspectives on the Tertiary Prevention Strategy for Alzheimer’s Disease, Current Alzheimer Research 2016; 13 (3) . https://dx.doi.org/10.2174/1567205013666151215110114
DOI https://dx.doi.org/10.2174/1567205013666151215110114 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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