In a recent review (23/10/23) published in the Journal of Neurochemistry, researchers evaluated the impact of the coronavirus disease 2019 (COVID-19) on Alzheimer’s disease (AD) pathology. They found that COVID-19 and Alzheimer’s disease (AD) share many risk factors and pathological characteristics. Both involve neuroinflammation that can damage neurons. This has raised concerns that SARS-CoV-2 infection may impact AD onset and progression.
AD is characterized by amyloid beta plaques, tau neurofibrillary tangles, inflammation, and neuron loss in brain regions like the hippocampus. Risk factors like age, diabetes, and genetics also increase COVID-19 severity.
Studies show SARS-CoV-2 infections are associated with greater cognitive decline and neurodegenerative disease risk. The virus appears to have amyloidogenic properties, increasing amyloid beta aggregation and toxicity.
SARS-CoV-2 entry and replication stimulate inflammatory cytokine release that can drive amyloid deposition and neurodegeneration. Virus-induced ACE2 inhibition also reduces BDNF, which protects neurons.
Post-mortem brain analyses of COVID-19 patients exhibit immune cell infiltration, blood-brain barrier disruption, axon damage, and astrocyte/microglia activation indicative of neuroinflammation.
In summary, the synergistic effects of COVID-19 and AD highlight the potential for SARS-CoV-2 infections to heighten inflammation and neurodegeneration linked to cognitive impairment. More research is needed on their long-term neurological implications.
You can read the full review here.