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Updated: Jul 19, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Clearance of amyloid-beta in Alzheimer's disease: progress, problems and perspectives
Yan-Jiang Wang1, Hua-Dong Zhou, Xin-Fu Zhou
1Department of Human Physiology and Centre for Neuroscience, Flinders University, Adelaide 5042, Australia.
Abstract:
Alzheimer's disease (AD) is the most common form of senile dementia and the fourth highest cause of disability and death in the elderly. Amyloid-beta (Abeta) has been widely implicated in the etiology of AD. Several mechanisms have been proposed for Abeta clearance, including receptor-mediated Abeta transport across the blood-brain barrier and enzyme-mediated Abeta degradation. Moreover, pre-existing immune responses to Abeta might also be involved in Abeta clearance. In AD, such mechanisms appear to have become impaired. Recently, therapeutic approaches for Abeta clearance, targeting immunotherapy and molecules binding Abeta, have been developed. In this review, we discuss recent progress and problems with respect to Abeta clearance mechanisms and propose strategies for the development of therapeutics targeting Abeta clearance.
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