Mohammad Azizur Rahman1*, Kamrul Islam1, Saidur Rahman2 and Al Amin3
1Department of Biochemistry and Molecular Biology, Jahangirnagar University, Savar, Dhaka, Bangladesh
2Department of Chemistry, Jahangirnagar University, Savar, Dhaka, Bangladesh
3Global Center for Environmental Remediation (GCER), The University of Newcastle, Callaghan, NSW, Australia
*Corresponding Author: Mohammad Azizur Rahman, Department of Biochemistry and Molecular Biology, Jahangirnagar University, Savar, Dhaka, Bangladesh.
Received: August 19, 2020; Published: September , 2020
COVID-19, the global threat to the humanity, shares etiological cofactors with multiple diseases including Alzheimer’s disease (AD). Understanding the common links between COVID-19 and AD would harness strategizing therapeutic approaches against both. Considering the urgency of formulating COVID-19 medication, its AD association and manifestations have been reviewed here, putting emphasis on memory and learning disruption. COVID-19 and AD share common links with respect to angiotensin-converting enzyme 2 (ACE2) receptors, proinflammatory markers such as interleukin-1 (IL-1), IL-6, cytoskeleton-associated protein 4 (CKAP4), galactein-9 and APOE4 allele. Common etiological factors and common manifestations described in this review would aid in developing therapeutic strategies for both COVID-19 and AD and thus impact on eradicating the ongoing global threat. Thus, people suffering from COVID-19 or who have come round of it as well as people at risk of developing AD or already suffering from AD, would be benefitted.
Keywords: ACE2; ApoE4; Gal-9; Inflammation; Neuroinvasive
Citation: Mohammad Azizur Rahman., et al. “Neurobiochemical Crosstalk between COVID-19 and Alzheimer’s Disease". Acta Scientific Neurology 3.10 (2020): .
Copyright: © 2020 Mohammad Azizur Rahman., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.