Molecular and cellular similarities identified in the brains of SARS-CoV-2 and Alzheimer's disease patients biorxivpreprint IcahnMountSinai SARSCoV2 COVID19 AlzheimersDisease
By Neha MathurNov 28 2022Reviewed by Aimee Molineux In a recent study posted to the bioRxiv* preprint server, researchers evaluated neuro-pathophysiological consequences of severe acute respiratory syndrome coronavirus 2 infection, especially the post-acute sequelae of SARS-CoV-2 in Alzheimer’s disease patients.
Likewise, all AD individuals had postmortem ABC scores indicative of AD, where A is a measure of amyloid-beta deposition. Likewise, B and C scores are measures of neurofibrillary degeneration based on the Braak and Brook score and neuritic plaques outlined by the Consortium to Establish a Registry for AD diagnosis , respectively.
Study findings Compared to neurological control brains, microglia in AD, SARS-CoV-2, and SARS-CoV-2 infected AD cases were more numerous, accumulated around blood vessels, and displayed retracted, thickened processes and enlarged somas, suggesting factors at the level of the BBB might be participating in microglial activation. The researchers found microglial nodules in all groups, but they appeared larger and more frequent in SARS-CoV-2 infected than in AD and control groups.
Further, the increased nodular formation in SARS-CoV-2-infected AD cases led to increased toll-like receptor signaling and upregulation of inflammasome genes. It led to T cell stimulation and the destruction of neurons, suggesting SARS-CoV-2 further promoted neuroinflammation in AD, which likely advanced the progression and severity of CNS disease in these individuals. Consistent with the findings of Zhou et al.
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