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SARS-CoV-2-Mediated Neuropathogenesis, Deterioration of Hippocampal Neurogenesis and Dementia
Author(s) -
Risna Kanjirassery Radhakrishnan,
Mahesh Kandasamy
Publication year - 2022
Publication title -
american journal of alzheimer's disease and other dementias
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.653
H-Index - 60
eISSN - 1938-2731
pISSN - 1533-3175
DOI - 10.1177/15333175221078418
Subject(s) - neuroinflammation , neurogenesis , neurocognitive , neuroscience , hippocampal formation , hippocampus , dementia , neuroplasticity , psychology , microglia , medicine , cognition , inflammation , pathology , immunology , disease
A significant portion of COVID-19 patients and survivors display marked clinical signs of neurocognitive impairments. SARS-CoV-2-mediated peripheral cytokine storm and its neurotropism appear to elicit the activation of glial cells in the brain proceeding to neuroinflammation. While adult neurogenesis has been identified as a key cellular basis of cognitive functions, neuroinflammation-induced aberrant neuroregenerative plasticity in the hippocampus has been implicated in progressive memory loss in ageing and brain disorders. Notably, recent histological studies of post-mortem human and experimental animal brains indicate that SARS-CoV-2 infection impairs neurogenic process in the hippocampus of the brain due to neuroinflammation. Considering the facts, this article describes the prominent neuropathogenic characteristics and neurocognitive impairments in COVID-19 and emphasizes a viewpoint that neuroinflammation-mediated deterioration of hippocampal neurogenesis could contribute to the onset and progression of dementia in COVID-19. Thus, it necessitates the unmet need for regenerative medicine for the effective management of neurocognitive deficits in COVID-19.

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