Table 1.

Potential mechanisms involved in Alzheimer’s Disease (AD) risk in COVID-19 patients.

Pathway	Mechanisms	References
Aβ deposition	Aβ is an antimicrobial peptide produced in response to neural infection as part of the innate immune innate response	[18,21,43]
APOEε4	APOEε4 represents a risk factor for both COVID-19 and AD; APOEε4 enhance the disruption of BBB; APOEε4 has an important role in neuroinflammation, which contributes to the pathogenic mechanism underlying AD.	[51,52]
Neuroinflammation	ACE-2 is expressed in the cells of the CNS; SARS-CoV-2 can infect cells within CNS; Pro-inflammatory cytokines can enter the CNS by crossing the altered BBB; Inflammatory response within CNS can alter cells within CNS leading to cognitive decline.	[25,27,28,29,42]
Microglia activation	SARS-CoV-2 infection can induce microglial activation leading to neuronal loss; Microglia activation promotes oxidative stress within brain; Increased NO levels are neurotoxic and promote AD development.	[30,41]

ACE-2: Angiotensin Converting Enzyme 2; AD: Alzheimer’s Disease; APOE: Apolipoprotein E; BBB: Blood Brain Barrier; COVID-19: Coronavirus Disease 2019; CSN: Central Nervous System; NO: Nitric Oxide; SARS-CoV-2: Severe Acute Respiratory Syndrome Coronavirus 2.