The functional and structural changes in the hippocampus of COVID-19 patients | SpringerLink
▻https://link.springer.com/article/10.1007/s13760-023-02291-1
Since the hippocampus is predominantly susceptible to injuries caused by COVID-19, there are increasing data indicating the likelihood of post-infection memory loss and quickening neurodegenerative disorders, such as Alzheimer’s disease. This is due to the fact that the hippocampus has imperative functions in spatial and episodic memory as well as learning. COVID-19 activates microglia in the hippocampus and induces a CNS cytokine storm, leading to loss of hippocampal neurogenesis. The functional and structural changes in the hippocampus of COVID-19 patients can explain neuronal degeneration and reduced neurogenesis in the human hippocampus. This will open a window to explain memory and cognitive dysfunctions in “long COVID” through the resultant loss of hippocampal neurogenesis.
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The proliferation and neuronal differentiation of neural stem cells can be suppressed by increased amounts of proinflammatory cytokines due to the pathogenic course of neurological disorders and anomalous amounts of stress hormones [5, 35, 108]. These factors can also interrupt the efficient incorporation of newborn neurons in the hippocampus in due course [5, 35, 108,109,110,111,112]. Impaired neurogenesis is known to be coupled with memory loss in neurological disorders due to neuroinflammation [3, 113]. This is also the case for COVID-19 where SARS-CoV-2 has the potential to infect neural stem cells in the hippocampus and brain organoids [3, 65, 108, 114, 115]. Clinical data also support the notion that Alzheimer’s disease can be initiated [116] or deteriorated [117] in COVID-19 patients.