**7. Adult neurogenesis in COVID-19**

Earlier studies show that survivors of critical illness have higher risk of developing neuropsychiatric consequences after discharge from the hospital. The prevalence of symptoms of depression, anxiety, and post-traumatic stress was found to be 29% [28–34], 34% [30–42], and 34% [27–50] in survivors of critical illness, respectively [70–72]. Impairment in memory, attention, and concentration was observed in SARS survivors 1 year after recovery [73]. Based on the knowledge from earlier infections by coronaviruses, SARS, and MERS, an increased risk of neuropsychiatric disorders like depression, anxiety, post-traumatic stress disorder, are possible in a long-term follow-up of patients recovered from COVID-19 [12].

Neuropsychiatric disorders that display impaired adult neurogenesis include major depressive disorder, Alzheimer's disease, Parkinson's disease, schizophrenia, and post-traumatic stress disorder. All of these correlate well with the reduction in hippocampal volume, cognitive deficits, and mood dysregulation [74]. A recent 3-month prospective study by Yiping Lu et al. conducted in COVID-19 recovered patients found that there was grey matter enlargement in olfactory cortices and hippocampus bilaterally [75]. Yiping Lu et al. also found that the grey matter volume of the hippocampus was negatively related to loss of smell during the disease phase [75]. Anosmia over a course of time in upper respiratory tract infections was found to be associated with a decrease in the grey matter volume [GMV] of the central olfactory system due to loss of stimulation while enlargement of GMV is observed during recovery [76]. Functional compensation in the form of enlarged neurons and an increase in the dendritic spine and compensatory enhanced neurogenesis are believed to be the reason behind GMV enlargement during recovery [77]. Loss of memory that persisted 3 months after the active infection in COVID-19 recovered patients was found to be negatively related to hippocampal grey matter volume [75]. Memory acquisition depends on newborn neurons and impairment in the acquisition of memory occurs due to inhibition of adult neurogenesis in the hippocampus [78, 79].

Anosmia is regarded as the key feature of COVID-19 which either occurs as an only symptom or in association with other signs and symptoms [80, 81]. Earlier studies show that any impairment in olfactory neurogenesis is associated with anosmia since neurogenesis in the olfactory epithelium and olfactory bulb is essential for the sense of smell [82, 83]. Dysfunction or atrophy of the olfactory bulb was observed in COVID-19 patients by recent studies done using brain imaging reports [84, 85]. Pathogenic changes in COVID-19 seem to cause loss of dopaminergic neurons, defects in the dopamine system, and exacerbate the clinical features of Parkinson's disease [PD] [86, 87]. Anosmia is an important premotor symptom of PD which is not directly related to the neurodegenerative process in substantia nigra but appears to be related to defective adult neurogenesis [88, 89].

Understanding the process of adult neurogenesis in COVID-19 may reveal a critical role of the regenerative capacity of NPCs in combating the neuropsychiatric consequence of COVID-19. There are no studies or evidence to link COVID-19 with adult neurogenesis yet. Based on the factors like the presentation of neuropsychiatric symptoms in COVID-19, the occurrence of symptoms like anosmia, memory and

#### *Does COVID-19 Affect Adult Neurogenesis? A Neurochemical Perspective DOI: http://dx.doi.org/10.5772/intechopen.101179*

cognitive deficits in COVID-19, the neuro-invasive potential of SARS-CoV-2, ACE2 expression in sites of adult neurogenesis, increased levels of pro-inflammatory cytokines like IL-6, Il-1β which inhibit adult neurogenesis and impact of earlier coronavirus infections, it might not be far-fetched to say that COVID-19 could have a possible impact on adult neurogenesis. There is a severe scarcity in research analysing the effect of SARS-CoV-2 infection on adult neurogenesis. The current chapter, which is speculative and based on a thorough literature search, discusses the possible changes in adult neurogenesis in COVID-19 emphasising the role of ACE2. If proven to be true in the future, the findings in this article will help in achieving early intervention to address the neuropsychiatric long-term consequence of COVID-19.
