SARS-CoV-2-Mediated Neuropathogenesis, Deterioration of Hippocampal Neurogenesis and Dementia.
Risna K RadhakrishnanMahesh KandasamyPublished in: American journal of Alzheimer's disease and other dementias (2022)
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.
Keyphrases
- cerebral ischemia
- sars cov
- subarachnoid hemorrhage
- respiratory syndrome coronavirus
- blood brain barrier
- brain injury
- coronavirus disease
- mild cognitive impairment
- cognitive impairment
- bipolar disorder
- endothelial cells
- induced apoptosis
- traumatic brain injury
- multiple sclerosis
- spinal cord injury
- high glucose
- diabetic rats
- oxidative stress
- drug induced
- white matter
- lipopolysaccharide induced
- cell death
- signaling pathway
- induced pluripotent stem cells
- childhood cancer