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Perspectives on the Tertiary Prevention Strategy for Alzheimer's Disease
Xian-Le Bu, Shu-Sheng Jiao, Yan Lian
1Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China. yanjiang_wang@tmmu.edu.cn.
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.
Insights
Alzheimer's disease (AD) treatments targeting only amyloid-beta (Aβ) have failed. New strategies must address multiple pathways and disease stages, drawing inspiration from stroke management.
Area of Science:
- Neuroscience
- Pathology
- Pharmacology
Background:
- Amyloid-beta (Aβ) is a key target in Alzheimer's disease (AD) research.
- Numerous clinical trials targeting Aβ have yielded disappointing results, questioning its sole efficacy.
- AD pathogenesis involves complex interactions including tau hyperphosphorylation, oxidative stress, and neuroinflammation.
Purpose of the Study:
- To re-evaluate current therapeutic targets for Alzheimer's disease.
- To explore novel intervention strategies beyond single-target approaches.
- To investigate the potential of tertiary prevention strategies, inspired by ischemic stroke management, for AD.
Main Methods:
- Review of existing literature on AD pathogenesis and therapeutic failures.
- Analysis of pathophysiological similarities between Alzheimer's disease and ischemic stroke.
- Conceptualization of a multi-target, stage-specific therapeutic approach.
Main Results:
- Aβ-centric therapies alone are insufficient for halting or reversing AD progression.
- AD pathology is multifactorial and progresses differently across disease stages.
- Successful ischemic stroke management offers a model for AD tertiary prevention.
Conclusions:
- Targeting Aβ exclusively is inadequate for effective AD treatment.
- A comprehensive strategy addressing multiple pathological pathways at different disease stages is necessary.
- Tertiary prevention strategies, integrating Aβ and other pathways, show promise for AD treatment and prevention.
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