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Amyloid Beta: The Foremost Protagonist in Alzheimer's Disease
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Author(s): Abhinav Anand (Lovely Professional University, India), Neha Sharma (Lovely Professional University, India), Monica Gulati (Lovely Professional University, India)and Navneet Khurana (Lovely Professional University, India)
Copyright: 2019
Pages: 17
Source title:
Handbook of Research on Critical Examinations of Neurodegenerative Disorders
Source Author(s)/Editor(s): Md. Sahab Uddin (Southeast University, Bangladesh)and Md. Shah Amran (University of Dhaka, Bangladesh)
DOI: 10.4018/978-1-5225-5282-6.ch011
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Abstract
Alzheimer's disease (AD), exhibiting accumulation of amyloid beta (Aβ) peptide as a foremost protagonist, is one of the top five causes of deaths. It is a neurodegenerative disorder (ND) that causes a progressive decline in memory and cognitive abilities. It is characterized by deposition of Aβ plaques and neurofibrillary tangles (NFTs) in the neurons, which in turn causes a decline in the brain acetylcholine levels. Aβ hypothesis is the most accepted hypothesis pertaining to the pathogenesis of AD. Amyloid Precursor Protein (APP) is constitutively present in brain and it is cleaved by three proteolytic enzymes (i.e., alpha, beta, and gamma secretases). Beta and gamma secretases cleave APP to form Aβ. Ubiquitin Proteasome System (UPS) is involved in the clearing of Aβ plaques. AD also involves impairment in UPS. The novel disease-modifying approaches involve inhibition of beta and gamma secretases. A number of clinical trials are going on worldwide with moieties targeting beta and gamma secretases. This chapter deals with an overview of APP and its enzymatic cleavage leading to AD.
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