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10.1002/jcp.29937

http://scihub22266oqcxt.onion/10.1002/jcp.29937
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32697344!7405062!32697344
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suck abstract from ncbi


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pmid32697344      J+Cell+Physiol 2021 ; 236 (2): 763-770
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  • COVID-19 and olfactory dysfunction: A possible associative approach towards neurodegenerative diseases #MMPMID32697344
  • Mahalaxmi I; Kaavya J; Mohana Devi S; Balachandar V
  • J Cell Physiol 2021[Feb]; 236 (2): 763-770 PMID32697344show ga
  • The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the agent of novel coronavirus 2019 (COVID-19), has kept the globe in disquiets due to its severe life-threatening conditions. The most common symptoms of COVID-19 are fever, sore throat, and shortness of breath. According to the anecdotal reports from the health care workers, it has been suggested that the virus could reach the brain and can cause anosmia, hyposmia, hypogeusia, and hypopsia. Once the SARS-CoV-2 has entered the central nervous system (CNS), it can either exit in an inactive form in the tissues or may lead to neuroinflammation. Here, we aim to discuss the chronic infection of the olfactory bulb region of the brain by SARS-CoV-2 and how this could affect the nearby residing neurons in the host. We further review the probable cellular mechanism and activation of the microglia 1 phenotype possibly leading to various neurodegenerative disorders. In conclusion, SARS-CoV-2 might probably infect the olfactory bulb neuron enervating the nasal epithelium accessing the CNS and might cause neurodegenerative diseases in the future.
  • |*SARS-CoV-2[MESH]
  • |Animals[MESH]
  • |COVID-19/*complications[MESH]
  • |Humans[MESH]
  • |Neurodegenerative Diseases/etiology[MESH]


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