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Exposure to Environmental Arsenic and Emerging Risk of Alzheimer’s Disease: Perspective Mechanisms, Management Strategy, and Future Directions

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Department of Pathology, College of Korean Medicine, Kyung Hee University, 1-5 Hoegidong Dongdaemungu, Seoul 02447, Korea
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Korean Medicine-Based Drug Repositioning Cancer Research Center, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea
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Global Biotechnology & Biomedical Research Network (GBBRN), Department of Biotechnology and Genetic Engineering, Faculty of Biological Sciences, Islamic University, Kushtia 7003, Bangladesh
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ABEx Bio-Research Center, East Azampur, Dhaka 1230, Bangladesh
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Department of Biochemistry and Molecular Biology, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh
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Graduate School of Pharmaceutical Sciences, College of Pharmacy, Ewha Womans University, Seoul 03760, Korea
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Department of Animal Science & Technology and BET Research Institute, Chung-Ang University, Anseong 17546, Korea
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Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine and Hospital, Seoul 03080, Korea
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Authors to whom correspondence should be addressed.
Academic Editor: Michael Aschner
Toxics 2021, 9(8), 188; https://doi.org/10.3390/toxics9080188
Received: 14 July 2021 / Revised: 11 August 2021 / Accepted: 11 August 2021 / Published: 14 August 2021
(This article belongs to the Special Issue Neurotoxicity of Environmental Metal Toxicants)
Alzheimer’s disease (AD) is one of the most prevailing neurodegenerative diseases, characterized by memory dysfunction and the presence of hyperphosphorylated tau and amyloid β (Aβ) aggregates in multiple brain regions, including the hippocampus and cortex. The exact etiology of AD has not yet been confirmed. However, epidemiological reports suggest that populations who were exposed to environmental hazards are more likely to develop AD than those who were not. Arsenic (As) is a naturally occurring environmental risk factor abundant in the Earth’s crust, and human exposure to As predominantly occurs through drinking water. Convincing evidence suggests that As causes neurotoxicity and impairs memory and cognition, although the hypothesis and molecular mechanism of As-associated pathobiology in AD are not yet clear. However, exposure to As and its metabolites leads to various pathogenic events such as oxidative stress, inflammation, mitochondrial dysfunctions, ER stress, apoptosis, impaired protein homeostasis, and abnormal calcium signaling. Evidence has indicated that As exposure induces alterations that coincide with most of the biochemical, pathological, and clinical developments of AD. Here, we overview existing literature to gain insights into the plausible mechanisms that underlie As-induced neurotoxicity and the subsequent neurological deficits in AD. Prospective strategies for the prevention and management of arsenic exposure and neurotoxicity have also been discussed. View Full-Text
Keywords: arsenic; Alzheimer’s disease (AD); environmental risk factor; mitochondrial dysfunction; proteostasis; apoptosis; phytochemicals arsenic; Alzheimer’s disease (AD); environmental risk factor; mitochondrial dysfunction; proteostasis; apoptosis; phytochemicals
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MDPI and ACS Style

Rahman, M.A.; Hannan, M.A.; Uddin, M.J.; Rahman, M.S.; Rashid, M.M.; Kim, B. Exposure to Environmental Arsenic and Emerging Risk of Alzheimer’s Disease: Perspective Mechanisms, Management Strategy, and Future Directions. Toxics 2021, 9, 188. https://doi.org/10.3390/toxics9080188

AMA Style

Rahman MA, Hannan MA, Uddin MJ, Rahman MS, Rashid MM, Kim B. Exposure to Environmental Arsenic and Emerging Risk of Alzheimer’s Disease: Perspective Mechanisms, Management Strategy, and Future Directions. Toxics. 2021; 9(8):188. https://doi.org/10.3390/toxics9080188

Chicago/Turabian Style

Rahman, Md. A., Md. A. Hannan, Md J. Uddin, Md S. Rahman, Md M. Rashid, and Bonglee Kim. 2021. "Exposure to Environmental Arsenic and Emerging Risk of Alzheimer’s Disease: Perspective Mechanisms, Management Strategy, and Future Directions" Toxics 9, no. 8: 188. https://doi.org/10.3390/toxics9080188

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