COVID-19 and Alzheimer's Disease: A Review of Mechanisms and Pathophysiology

SARS‑CoV‑2 virus, which has emerged as a worldwide epidemic, is accompanied by systemic symptoms, such as fever, cough, shortness of breath, and body aches. The virus enters the central nervous system in various ways and causes symptoms, such as dizziness, headache, and loss of consciousness, encephalitis, demyelination, neuropathy, stroke, seizure, and memory loss. Infection of the virus into the nervous system, particularly the hippocampus, can cause memory impairment. On the other hand, hypoxia due to lung infection may have a role in the development or progression of Alzheimerchr('39')s disease (AD). An increase of beta-amyloid production, as well as autophagy following hypoxia, causes nerve damage. Furthermore, chronic hypoxia reduces the expression of beta-amyloid-degrading enzymes by increasing the expression of the beta-secretase enzyme. On the other hand, peripheral proinflammatory cytokines produced by microglia are involved in increasing beta-amyloid levels and tau hyperphosphorylation. Other possible mechanisms involved in the development of AD following the SARS‑CoV‑2 virus infection include mitochondrial disorders and increased oxidative stress, which play an important role in the pathophysiology of AD. Oxidative stress increases beta-amyloid production by reducing alpha-secretase activity.

The SARS‑CoV‑2 virus may exacerbate the symptoms of AD by entering directly into the central nervous system and damaging vital areas in-memory storage or the consequences of chronic hypoxia, oxidative stress, or increased production of peripheral proinflammatory cytokines.