Links between COVID-19 and Alzheimer’s Disease—What Do We Already Know?

Ewa Rudnicka-Drożak, Paulina Drożak (), Grzegorz Mizerski, Tomasz Zaborowski, Barbara Ślusarska, Grzegorz Nowicki and Martyna Drożak
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Ewa Rudnicka-Drożak: Chair and Department of Family Medicine, Medical University of Lublin, Langiewicza 6a, 20-035 Lublin, Poland
Paulina Drożak: Student Scientific Society, Chair and Department of Family Medicine, Medical University of Lublin, Langiewicza 6a, 20-035 Lublin, Poland
Grzegorz Mizerski: Chair and Department of Family Medicine, Medical University of Lublin, Langiewicza 6a, 20-035 Lublin, Poland
Tomasz Zaborowski: Chair and Department of Family Medicine, Medical University of Lublin, Langiewicza 6a, 20-035 Lublin, Poland
Barbara Ślusarska: Department of Family and Geriatric Nursing, Faculty of Health Sciences, Medical University of Lublin, 20-081 Lublin, Poland
Grzegorz Nowicki: Department of Family and Geriatric Nursing, Faculty of Health Sciences, Medical University of Lublin, 20-081 Lublin, Poland
Martyna Drożak: Student Scientific Society, Chair and Department of Family Medicine, Medical University of Lublin, Langiewicza 6a, 20-035 Lublin, Poland

IJERPH, 2023, vol. 20, issue 3, 1-15

Abstract: Alzheimer’s disease (AD) is a life-changing condition whose etiology is explained by several hypotheses. Recently, a new virus contributed to the evidence of viral involvement in AD: the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes the COVID-19 coronavirus disease. AD was found to be one of the most common COVID-19 comorbidities, and it was found to increase mortality from this disease as well. Moreover, AD patients were observed to present with the distinct clinical features of COVID-19, with delirium being prevalent in this group. The SARS-CoV-2 virus enters host cells through the angiotensin-converting enzyme 2 (ACE2) receptor. ACE2 is overexpressed in brains with AD, which thus increases the viral invasion. Furthermore, the inhibition of the ACE2 receptor by the SARS-CoV-2 virus may also decrease the brain-derived neurotrophic factor (BDNF), contributing to neurodegeneration. The ApoE ε4 allele, which increases the risk of AD, was found to facilitate the SARS-CoV-2 entry into cells. Furthermore, the neuroinflammation and oxidative stress existing in AD patients enhance the inflammatory response associated with COVID-19. Moreover, pandemic and associated social distancing measures negatively affected the mental health, cognitive function, and neuro-psychiatric symptoms of AD patients. This review comprehensively covers the links between COVID-19 and Alzheimer’s disease, including clinical presentation, molecular mechanisms, and the effects of social distancing.

Keywords: Alzheimer’s disease; COVID-19; SARS-CoV-2; neuroinflammation (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2023
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