 Corresponding author: S P Srinivas Nayak, Email id: spnayak843@gmail.com Assistant Professor, Dept. of Pharmacy Practice, Parul Institute of Pharmacy and Research, Parul University, Vadodara, Gujarat Copyright © 2021 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution Liscense 4.0. Drug information of Aducanumab and its effectiveness for Alzheimer’s disease: A clinical review Neel Sureshbhai Raval 1 , Sachi Anilkumar Chavda 1 , Dhwanil Nileshkumar Mithaiwala 1 , SP Srinivas Nayak 2, * , Mohit Buddhdev 2 and Gunosindhu Chakraborthy 3 1 Parul Institute of Pharmacy and Research, Parul University, Vadodara, Gujarat. 2 Dept. of Pharmacy Practice, Parul Institute of Pharmacy and Research, Parul University, Vadodara, Gujarat. 3 Prof. and Principal, Parul Institute of Pharmacy and Research, Parul University, Vadodara, Gujarat. International Journal of Biological and Pharmaceutical Sciences Archive, 2021, 02(02), 072–077 Publication history: Received on 27 October 2021; revised on 20 December 2021; accepted on 22 December 2021 Article DOI: https://doi.org/10.53771/ijbpsa.2021.2.2.0094 Abstract Alzheimer’s disease (AD) is the main cause of disability in people older than 60 years. More than 1 million cases per year reported in India. AD and other kinds of dementia are more common as individuals become older, affecting 1 in every 14 people over the age of 65 and 1 in every 6 people over the age of 80. ADUHELM (Aducanumab) is a monoclonal antibody, new class of medication needed for treatment of AD. The latest drug used to treat underlying cause of AD and recent studies shown to be efficacious and safe for the AD. Our review emphasizes on the drug information of Aducanumab and its clinical importance in AD. Keywords: Alzheimer’s disease; Aducanumab; Drug information; Genetic mutations. 1. Introduction Early onset Alzheimer disease (EOAD) is a neurodegenerative dementing disorder that is relatively rare (<1% of all Alzheimer cases). Various genetic mutations of the presenilin 1 (PSEN1) and presenilin 2 (PSEN2) as well as the amyloid precursor protein (APP) gene have been implicated. Mutations of PSEN1 and PSEN2 alter γ -secretase enzyme that cleaves APP resulting in increase in the relative amount of the more amyloidogenic Aβ42 that is produced. [1] AD is a neurodegenerative condition that causes brain shrinkage and cell death overtime.[2] PSEN2 mutations are reported to be associated with AD of both early onset and variable age onset as well as with other neurodegenerative disorders such as Lewy Body dementia, frontotemporal dementia, Parkinson dementia, and posterior cortical atrophy[2-4].; Patients most often present with an insidious loss of episodic memory followed by a slowly progressive dementia that evolves over years.[3] AD is the most common cause of dementia, which is characterised by a progressive loss of cognitive, behavioural, and social abilities that impairs a person's capacity to operate independently.[1] Dementia is described as a group of symptoms affecting severely to thinking, memory, and social abilities which may interfere with your day-to- day life.[4] AD establishes around 70% of all dementia cases. AD is typically an old age disease. The global prevalence of dementia is about 24 million and it’s going to increase 4 times by 2050. AD is expected to cost $172 billion a year in health-care costs in the United States alone. The incidence rate of AD after the age of 65 is multiplied by 5 times. Age- specific incidence increases significantly from less than 1% per year before 65 years of age to 6% per year after 85 years of age. Prevalence rates increase from 10% after the age of 65 to 40 % after the age of 85. Women are somewhat more likely than males to get AD, especially beyond the age of 85. To date, most validated research results have been narrowed down to yield a model for biological trajectory of AD, where amyloid deposition far precedes clinical symptoms. [5]. Old age and a favourable family history are the two most major risk factors for AD. The prevalence of AD increases with each decade of adult life, reaching 20–40% of the population over the age of 85. A positive family history of dementia