Alzheimer's-like signaling in brains of COVID-19 patients.
Alzheimers Dement
; 18(5): 955-965, 2022 05.
Article
in English
| MEDLINE | ID: covidwho-1669366
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-ß 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.Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Alzheimer Disease
/
COVID-19
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Alzheimers Dement
Year:
2022
Document Type:
Article
Affiliation country:
Alz.12558
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