{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Green R"],"funding":["BLRD VA","NCI NIH HHS","NINDS NIH HHS"],"pagination":["217-229"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9508696"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27"],"pubmed_abstract":["The coronavirus disease 2019 (COVID-19) pandemic has caused over 600,000,000 infections globally thus far. Up to 30% of individuals with mild to severe disease develop long COVID, exhibiting diverse neurologic symptoms including dementias. However, there is a paucity of knowledge of molecular brain markers and whether these can precipitate the onset of Alzheimer's disease (AD). Herein, we report the brain gene expression profiles of severe COVID-19 patients showing increased expression of innate immune response genes and genes implicated in AD pathogenesis. The use of a mouse-adapted strain of SARS-CoV-2 (MA10) in an aged mouse model shows evidence of viral neurotropism, prolonged viral infection, increased expression of tau aggregator FKBP51, interferon-inducible gene <i>Ifi204</i>, and complement genes C4 and C5AR1. Brain histopathology shows AD signatures including increased tau-phosphorylation, tau-oligomerization, and α-synuclein expression in aged MA10 infected mice. The results of gene expression profiling of SARS-CoV-2-infected and AD brains and studies in the MA10 aged mouse model taken together, for the first time provide evidence suggesting that SARS-CoV-2 infection alters expression of genes in the brain associated with the development of AD. Future studies of common molecular markers in SARS-CoV-2 infection and AD could be useful for developing novel therapies targeting AD."],"journal":["Molecular therapy. Methods & clinical development"],"pubmed_title":["SARS-CoV-2 infection increases the gene expression profile for Alzheimer's disease risk."],"pmcid":["PMC9508696"],"funding_grant_id":["R01 NS073899","IK6 BX004214","IK6 BX004212","I01 BX005490","R01 CA180758","I01 BX005757","I01 BX004626"],"pubmed_authors":["Chandran B","Mohapatra S","Green R","Mayilsamy K","Mohapatra SS","Martinez TE","McGill AR","Bickford PC","Blair LJ"],"additional_accession":[]},"is_claimable":false,"name":"SARS-CoV-2 infection increases the gene expression profile for Alzheimer's disease risk.","description":"The coronavirus disease 2019 (COVID-19) pandemic has caused over 600,000,000 infections globally thus far. Up to 30% of individuals with mild to severe disease develop long COVID, exhibiting diverse neurologic symptoms including dementias. However, there is a paucity of knowledge of molecular brain markers and whether these can precipitate the onset of Alzheimer's disease (AD). Herein, we report the brain gene expression profiles of severe COVID-19 patients showing increased expression of innate immune response genes and genes implicated in AD pathogenesis. The use of a mouse-adapted strain of SARS-CoV-2 (MA10) in an aged mouse model shows evidence of viral neurotropism, prolonged viral infection, increased expression of tau aggregator FKBP51, interferon-inducible gene <i>Ifi204</i>, and complement genes C4 and C5AR1. Brain histopathology shows AD signatures including increased tau-phosphorylation, tau-oligomerization, and α-synuclein expression in aged MA10 infected mice. The results of gene expression profiling of SARS-CoV-2-infected and AD brains and studies in the MA10 aged mouse model taken together, for the first time provide evidence suggesting that SARS-CoV-2 infection alters expression of genes in the brain associated with the development of AD. Future studies of common molecular markers in SARS-CoV-2 infection and AD could be useful for developing novel therapies targeting AD.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2026-05-28T06:36:58.994Z","creation":"2024-11-07T00:36:52.396Z"},"accession":"S-EPMC9508696","cross_references":{"pubmed":["36187720"],"doi":["10.1016/j.omtm.2022.09.007"]}}