Molecular and Therapeutic Targets for Amyloid-beta Plaques in Alzheimer's Disease: A Review Study

Abstract

Alzheimer’s disease (AD) is characterized by progressive loss of cognition and a gradual decrease in memory. Though AD is considered the most persistent form of dementia and a global concern, no complete cure or agents that can completely halt the progression of AD have been found. In the past years, considerable advancements in the understanding of cellular and molecular changes associated with AD has been investigated and numerous pharmacological targets have been recognized to enable drug development for the condition. Amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFT) are the major attributes of AD. Symptomatic relief is the only possible treatment available at present and a disease modifying drug is of utmost importance. Development of drugs that can inhibit different targets responsible for the formation of plaques is a potential area in AD research. This review is not a complete list of all possible targets for AD but serves to highlight the targets related to amyloid pathology and pathway concerned with the formation of amyloid fragments. This shall serve as a prospect in identification of amyloid plaque inhibitors and pave the strategies for newer drug treatments. Nevertheless, substantial research is done in this area but to bridle, the clinical difficulty remains a concern.