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

Alzheimer’s disease (AD) is characterized by progressive loss of cognition and a gradual decrease in memory. Although 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, significant progress has been made in understanding the cellular and molecular changes associated with AD, and numerous drug targets have been identified for the development of drugs for this disease. 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. The 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 Aβ pathology and pathways concerned with the formation of Aβ fragments. This shall serve as a prospect in the identification of Aβ 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.