Alzheimer's disease; a review of the pathophysiological basis and therapeutic interventions
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Updated: Dec 17, 2025

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
A A D T Abeysinghe1, R D U S Deshapriya2, C Udawatte3
1College of Chemical Sciences, Institute of Chemistry Ceylon, Rajagiriya, Sri Lanka; Department of Chemistry, Faculty of Applied Sciences, University of Sri Jayewardenepura, Nugegoda, Sri Lanka.
Abstract:
Alzheimer's disease (AD) is a neurodegenerative disorder and is identified as the most common cause for dementia. Despite huge global economic burden and the impact on the close family of the patients, there is no definitive cure and thus, improved treatment methods are of need. While memory and cognition are severely affected in AD, exact etiology is yet unknown. The β-Amyloid plaque formation and aggregation hypothesis is among the well-known hypotheses used to explain disease pathogenesis. Currently there are five Food and Drug Administration (FDA) approved drugs as treatment options. All these drugs are used for symptomatic treatment of AD. Thus, disease modifying therapies which can directly address the pathological changes in AD, are needed. Such therapies could be designed based on inhibiting key steps of pathogenesis. Currently there are novel AD drug candidates with various therapeutic mechanisms, undergoing different stages of drug development. Extensive research is being done globally to broaden understanding of the exact mechanisms involved in AD and to develop therapeutic agents that can successfully hinder the occurrence and progression of the disease. In this review, a comprehensive approach to understanding AD and suggestions to be considered in the development of therapeutics for it are presented.
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