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.

很大一部分 COVID-19 患者和幸存者表现出明显的神经认知障碍临床症状。 SARS-CoV-2 介导的外周细胞因子风暴及其向神经性似乎会引发大脑中神经胶质细胞的激活，从而导致神经炎症。虽然成人神经发生已被确定为认知功能的关键细胞基础，但神经炎症引起的海马异常神经再生可塑性与衰老和脑部疾病中的进行性记忆丧失有关。值得注意的是，最近对死后人类和实验动物大脑的组织学研究表明，SARS-CoV-2 感染会因神经炎症而损害大脑海马体的神经发生过程。考虑到事实，本文描述了 COVID-19 的突出神经病理特征和神经认知障碍，并强调了这样一种观点，即神经炎症介导的海马神经发生恶化可能导致 COVID-19 痴呆的发生和进展。因此，为了有效管理 COVID-19 的神经认知缺陷，再生医学的需求尚未得到满足。