APOE4: A Culprit for the Vulnerability of COVID-19 in Alzheimer's Patients.

Autor:	Goyal A; Institute of Pharmaceutical Research, GLA University, Mathura, U.P., India., Kushwah PS; Department of Pharmaceutical Sciences, Maharshi Dayanand University, Rohtak, Haryana, India., Agrawal N; Institute of Pharmaceutical Research, GLA University, Mathura, U.P., India., Pathak S; Institute of Pharmaceutical Research, GLA University, Mathura, U.P., India.
Jazyk:	angličtina
Zdroj:	Current neurovascular research [Curr Neurovasc Res] 2023; Vol. 20 (1), pp. 162-169.
DOI:	10.2174/1567202620666230202140612
Abstrakt:	Apolipoprotein E4 (APOE4) is one of the primary genetic risk factors for late-onset of Alzheimer's disease (AD). While its primary function is to transport cholesterol, it also regulates metabolism, aggregation, and deposition of amyloid-β (Aβ) in the brain. The disruption in the generation and removal of Aβ in the brain is the primary cause of memory and cognitive loss and thus plays a significant role in the development of AD. In several prior genetic investigations, the APOE4 allele has been linked to higher susceptibility to severe acute respiratory syndrome (SARSCoV- 2) infection and COVID-19 mortality. However, information on the involvement of APOE4 in the underlying pathology and clinical symptoms is limited. Due to the high infection and mortality rate of COVID-19 in AD individuals, challenges have been identified in the management of AD patients during the COVID-19 pandemic. In order to provide evidence-based, more effective healthcare, it is critical to identify underlying concerns and, preferably, biomarkers. The risk variant APOE4 imparts enhanced infectivity by the underlying coronavirus SARS-CoV-2 at a cellular level, genetic level, and route level. Here we review existing advances in clinical and basic research on the AD-related gene APOE, as well as the role of APOE in AD pathogenesis, using neurobiological evidence. Moreover, the role of APOE in severe COVID-19 in Alzheimer's patients has also been reviewed. (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
Databáze:	MEDLINE
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