Since December 2019, humankind has been experiencing a ravaging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak, the second coronavirus pandemic in a decade after the Middle East respiratory syndrome coronavirus (MERS-CoV) disease in 2012. Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19), which is responsible for over 3.1 million deaths worldwide. With the emergence of a second and a third wave of infection across the globe, and the rising record of multiple reinfections and relapses, SARS-CoV-2 infection shows no sign of abating. In addition, it is now evident that SARS-CoV-2 infection presents with neurological symptoms that include early hyposmia, ischemic stroke, meningitis, delirium and falls, even after viral clearance. This may suggest chronic or permanent changes to the neurons, glial cells, and/or brain vasculature in response to SARS-CoV-2 infection or COVID-19. Within the central nervous system (CNS), microglia act as the central housekeepers against altered homeostatic states, including during viral neurotropic infections. In this review, we highlight microglial responses to viral neuroinfections, especially those with a similar genetic composition and route of entry as SARS-CoV-2. As the primary sensor of viral infection in the CNS, we describe the pathogenic and neuroinvasive mechanisms of RNA viruses and SARS-CoV-2 vis-à-vis the microglial means of viral recognition. Responses of microglia which may culminate in viral clearance or immunopathology are also covered. Lastly, we further discuss the implication of SARS-CoV-2 CNS invasion on microglial plasticity and associated long-term neurodegeneration. As such, this review provides insight into some of the mechanisms by which microglia could contribute to the pathophysiology of post-COVID-19 neurological sequelae and disorders, including Parkinson’s disease, which could be pervasive in the coming years given the growing numbers of infected and re-infected individuals globally.
Background: Air fresheners are products with fragrances used to mask unpleasant odor in the environment. However, air fresheners contain diverse chemical substances that pose health challenges to the users; hence are of public health significance. Although previous studies have shown that air fresheners affect the lungs, liver and reproductive organs, the neurobehavioral effects of these agents are yet to be evaluated in details. This study evaluated the neurobehavioral effects and biochemical changes in mice exposed to a solid commercially available air freshener (SAF). Methods: Male Swiss mice were divided into 6 groups (n = 7). Mice in groups 2-6 were exposed to powdered SAF (10, 25, 50, 100 and 200 g) via inhalation in their cages for 28 days. Mice in group 1 (control) were not exposed to SAF. The neurobehavioral changes: spontaneous motor activity (SMA), memory, anxiety and depression were evaluated on day 28. The mice brains were then proccessed for determination of malondialdehyde, nitrite, glutathione contents, and the activities of catalase and acetyl-cholinesterase. Results: SAF (25-200g) significantly (p<0.05) impaired SMA compared with control. Mice exposed to SAF exhibited increased anxiety and depression-like symptoms relative to control (p<0.05). It also impaired memory and increased acetylcholinesterase activity (p<0.05). Moreover, SAF increased the levels of nitrite and malondialdehyde accompanied by decreased antioxidant molecules (glutathione and catalase) in mouse brain. Conclusion: These findings suggest that SAF produced neurobehavioral deficits, increased oxidative stress and altered cholinergic system, posing potential health hazards to the regular consumers.
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