Alzheimer's disease; a review of the pathophysiological basis and therapeutic interventions

• Published in: Life sciences (1973) Vol. 256; p. 117996
• Main Authors: Abeysinghe, A.A.D.T., Deshapriya, R.D.U.S., Udawatte, C.
• Format: Journal Article
• Language: English
• Published: New York Elsevier Inc 01.09.2020; Elsevier BV
• Subjects: Acetylcholinesterase inhibitors; Alzheimer's disease; Chemical compounds; Cognition; Dementia disorders; Disease modifying therapy; Drug development; Drugs; Etiology; Hypotheses; Impact analysis; Medical treatment; Neurodegenerative diseases; Pathogenesis; Pathophysiology; Pharmacology; Therapeutic applications; β-Amyloid; Acetylcholinesterase inhibitors; Disease modifying therapy; Pathophysiology; Alzheimer's disease
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2020.117996

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. [Display omitted]