Exploring the Role of Monoamine Oxidase Activity in Aging and Alzheimer’s Disease

Author:

Rahman Md. Sohanur1,Uddin Md. Sahab2ORCID,Rahman Md. Ataur3,Samsuzzaman Md.4,Behl Tapan5,Hafeez Abdul6,Perveen Asma7,Barreto George E.8,Ashraf Ghulam Md.9

Affiliation:

1. Department of Biochemistry and Molecular Biology, Trust University, Barishal, Ruiya, Nobogram Road, Barishal 8200, Bangladesh

2. Department of Pharmacy, Southeast University, Dhaka, Bangladesh

3. Center for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Korea

4. Department of Food and Life Science, Pukyong National University, Busan 48513, Korea

5. Chitkara College of Pharmacy, Chitkara University, Punjab, India

6. Glocal School of Pharmacy, Glocal University, Saharanpur, India

7. Glocal School of Life Sciences, Glocal University, Saharanpur, India

8. Department of Biological Sciences, University of Limerick, Limerick, Ireland

9. Pre-Clinical Research Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia

Abstract

Monoamine oxidases (MAOs) are a family of flavin adenine dinucleotide-dependent enzymes that have a crucial role in the metabolism of neurotransmitters of the central nervous system. Impaired function of MAOs is associated with copious brain diseases. The alteration of monoamine metabolism is a characteristics feature of aging. MAO plays a crucial role in the pathogenesis of Alzheimer’s disease (AD), a progressive neurodegenerative disorder associated with an excessive accumulation of amyloid-beta (Aβ) peptide and neurofibrillary tangles (NFTs). Activated MAO plays a critical role in the development of amyloid plaques from Aβ as well as the formation of the NFTs. In the brain, MAO mediated metabolism of monoamines is the foremost source of reactive oxygen species formation. The elevated level of MAO-B expression in astroglia has been reported in the AD brains adjacent to amyloid plaques. Increased MAO-B activity in the cortical and hippocampal regions is associated with AD. This review describes the pathogenic mechanism of MAOs in aging as well as the development and propagation of Alzheimer’s pathology.

Publisher

Bentham Science Publishers Ltd.

Subject

Drug Discovery,Pharmacology

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