Ontology highlight
ABSTRACT: Introduction
The mechanisms that lead to cognitive impairment associated with COVID-19 are not well understood.Methods
Brain lysates from control and COVID-19 patients were analyzed for oxidative stress and inflammatory signaling pathway markers, and measurements of Alzheimer's disease (AD)-linked signaling biochemistry. Post-translational modifications of the ryanodine receptor/calcium (Ca2+ ) release channels (RyR) on the endoplasmic reticuli (ER), known to be linked to AD, were also measured by co-immunoprecipitation/immunoblotting of the brain lysates.Results
We provide evidence linking SARS-CoV-2 infection to activation of TGF-β signaling and oxidative overload. The neuropathological pathways causing tau hyperphosphorylation typically associated with AD were also shown to be activated in COVID-19 patients. RyR2 in COVID-19 brains demonstrated a "leaky" phenotype, which can promote cognitive and behavioral defects.Discussion
COVID-19 neuropathology includes AD-like features and leaky RyR2 channels could be a therapeutic target for amelioration of some cognitive defects associated with SARS-CoV-2 infection and long COVID.
SUBMITTER: Reiken S
PROVIDER: S-EPMC9011576 | biostudies-literature | 2022 May
REPOSITORIES: biostudies-literature
Alzheimer's & dementia : the journal of the Alzheimer's Association 20220203 5
<h4>Introduction</h4>The mechanisms that lead to cognitive impairment associated with COVID-19 are not well understood.<h4>Methods</h4>Brain lysates from control and COVID-19 patients were analyzed for oxidative stress and inflammatory signaling pathway markers, and measurements of Alzheimer's disease (AD)-linked signaling biochemistry. Post-translational modifications of the ryanodine receptor/calcium (Ca2<sup>+</sup> ) release channels (RyR) on the endoplasmic reticuli (ER), known to be linked ...[more]