Attapon Cheepsattayakorn1,2*, Ruangrong Cheepsattayakorn3 and Porntep Siriwanarangsun1
1Faculty of Medicine, Western University, Pathumtani Province, Thailand
210th Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand
3Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand
*Corresponding Author: Attapon Cheepsattayakorn, 10th Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand.
Received: September 22, 2022; Published: October 01, 2022
SARS-CoV-2 (COVID-19) demonstrated decrease in the consciousness level [1]. Patients with Alzheimer’s disease (AD) experienced longer lockdown periods to protect themselves from being infected with COVID-19 or to recover from COVID-19 infection [2,3] that contributed to direct results (worse behavioral interferences and more severe neuropsychiatric symptoms) [3]. People with the mid-60’s of ages frequently present the most frequent type of AD that is not produced one gene only (apolipoprotein E gene (APOE)) [4]. Several hypothetically potential pathways are entry via the olfactory system [5,6], blood-brain barrier (BBB) [7,8], and COVID-19-infected-immune cell infiltration [9-11]. Smooth muscle cells in the brain blood vessels express angiotensin-converting-enzyme-2 receptors same as in the pulmonary alveolar cells [12]. Diabetes type 2 (T2D) is a risk factor for both AD and SARS-CoV-2 (COVID-19) via increased activity of interferon-regulatory-factor 5 (IRF5) (Figure 1) [13].
Citation: Attapon Cheepsattayakorn., et al. “Aging Adults with COVID-19 Infection and Alzheimer’s Disease". Acta Scientific Microbiology 5.11 (2022): 01-02.
Copyright: © 2022 Attapon Cheepsattayakorn., 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.