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10.1101/2022.01.31.478476 http://scihub22266oqcxt.onion/10.1101/2022.01.31.478476 35132414!8820661!35132414     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35132414&cmd=llinks): Failed to open stream: HTTP request failed! 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SARS-CoV-2 invades cognitive centers of the brain and induces Alzheimer s-like neuropathology |pdf=|usr=}}{{35132414}} gab.com Text SARS-CoV-2 invades cognitive centers of the brain and induces Alzheimer s-like neuropathology JO: bioRxiv http://www.kidney.de/pget.php?&tw=1&pmid=35132414 #FOAvip The neurotropism of SARS-CoV-2 and the phenotypes of infected neurons are still in debate. Long COVID manifests with "brain diseases" and the cause of these brain dysfunction is mysterious. Here, we analyze 34 age- and underlying disease-matched COVID-19 or non-COVID-19 human brains. SARS-CoV-2 RNA, nucleocapsid, and spike proteins are present in neurons of the cognitive centers of all COVID-19 patients, with its non-structural protein NSF2 detected in adult cases but not in the infant case, indicating viral replications in mature neurons. In adult COVID-19 patients without underlying neurodegeneration, SARS-CoV-2 infection triggers Abeta and p-tau deposition, degenerating neurons, microglia activation, and increased cytokine, in some cases with Abeta plaques and p-tau pretangles. The number of SARS-CoV-2 (+) cells is higher in patients with neurodegenerative diseases than in those without such conditions. SARS-CoV-2 further activates microglia and induces Abeta and p-tau deposits in non-Alzheimer's neurodegenerative disease patients. SARS-CoV-2 infects mature neurons derived from inducible pluripotent stem cells from healthy and Alzheimer's disease (AD) individuals through its receptor ACE2 and facilitator neuropilin-1. SARS-CoV-2 triggers AD-like gene programs in healthy neurons and exacerbates AD neuropathology. An AD infectious etiology gene signature is identified through SARS-CoV-2 infection and silencing the top three downregulated genes in human primary neurons recapitulates the neurodegenerative phenotypes of SARS-CoV-2. Thus, our data suggest that SARS-CoV-2 invades the brain and activates an AD-like program. Twit Text FOAVip SARS-CoV-2 invades cognitive centers of the brain and induces Alzheimer s-like neuropathology ????bioRxiv http://www.kidney.de/pget.php?&tw=1&pmid=35132414 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35132414 #FOAvip English Wikipedia <ref>{{Cite pmid|35132414}}</ref> SARS-CoV-2 invades cognitive centers of the brain and induces Alzheimer s-like neuropathology #MMPMID35132414 Shen WB; Elahi M; Logue J; Yang P; Baracco L; Reece EA; Wang B; Li L; Blanchard TG; Han Z; Rissman RA; Frieman MB; Yang P bioRxiv 2022[Sep]; ä (ä): ä PMID35132414show ga The neurotropism of SARS-CoV-2 and the phenotypes of infected neurons are still in debate. Long COVID manifests with "brain diseases" and the cause of these brain dysfunction is mysterious. Here, we analyze 34 age- and underlying disease-matched COVID-19 or non-COVID-19 human brains. SARS-CoV-2 RNA, nucleocapsid, and spike proteins are present in neurons of the cognitive centers of all COVID-19 patients, with its non-structural protein NSF2 detected in adult cases but not in the infant case, indicating viral replications in mature neurons. In adult COVID-19 patients without underlying neurodegeneration, SARS-CoV-2 infection triggers Abeta and p-tau deposition, degenerating neurons, microglia activation, and increased cytokine, in some cases with Abeta plaques and p-tau pretangles. The number of SARS-CoV-2 (+) cells is higher in patients with neurodegenerative diseases than in those without such conditions. SARS-CoV-2 further activates microglia and induces Abeta and p-tau deposits in non-Alzheimer's neurodegenerative disease patients. SARS-CoV-2 infects mature neurons derived from inducible pluripotent stem cells from healthy and Alzheimer's disease (AD) individuals through its receptor ACE2 and facilitator neuropilin-1. SARS-CoV-2 triggers AD-like gene programs in healthy neurons and exacerbates AD neuropathology. An AD infectious etiology gene signature is identified through SARS-CoV-2 infection and silencing the top three downregulated genes in human primary neurons recapitulates the neurodegenerative phenotypes of SARS-CoV-2. Thus, our data suggest that SARS-CoV-2 invades the brain and activates an AD-like program. äSARS-CoV-2 invades cognitive centers of the brain and induces Alzheime(epmc).pdf DeepDyve Pubget Overpricing