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

Int J Environ Res Public Health. 2023 Jan 25;20(3):2146. doi: 10.3390/ijerph20032146.

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.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease* / epidemiology
  • Angiotensin-Converting Enzyme 2
  • COVID-19* / epidemiology
  • Humans
  • Peptidyl-Dipeptidase A
  • SARS-CoV-2

Substances

  • Angiotensin-Converting Enzyme 2
  • Peptidyl-Dipeptidase A

Grants and funding

This research received no external funding.