Abstract

Alzheimer's disease is an insidious, slowly progressive neurodegenerative disease in aged people and the most prevalent form of dementia, characterized by loss of memory, behavioral changes, cognitive deterioration, and loss of functional abilities that affect the capability of a person to carry out daily tasks. The pathogenesis of AD is attributed to the accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain. Thus there is an urgent need for disease-modifying medication for its treatment. Conventional therapies like Acetylcholinesterase inhibitor and NMDAR antagonist are only used for symptomatic relief. Aducanumab is a human IgG1 monoclonal antibody that decreases plaque deposition by targeting accumulated insoluble and soluble forms of Aβ. Aducanumab was approved in June 07, 2021, by USFDA with the brand name ADUHELM as the first and only therapy to deal with a significant pathology of AD by lowering Aβ plaques in the brain. In this review, various aspects related to aducanumab have been summarized, including the pathophysiology of AD, pharmacological and non-pharmacological treatment of AD, mechanism as well as pharmacokinetics and pharmacodynamics of aducanumab, adverse reaction and various reported clinical trials. Aducanumab is a human IgG1 (immunoglobulin gamma1) monoclonal antibody that targets the aggregated, insoluble and soluble forms of Aβ and lowers the deposition of Aβ plaques in the brain. Aducanumab emerged as a potential drug to slow down the development of AD.

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