The recent outbreak of the novel coronavirus, SARS‐CoV‐2, has emerged to be highly pathogenic in nature. Although lungs are considered as the primary infected organs by SARS‐CoV‐2, some of the other organs, including the brain, have also been found to be affected. Here, we have discussed how SARS‐CoV‐2 might infect the brain. The infection of the respiratory center in the brainstem could be hypothesized to be responsible for the respiratory failure in many COVID‐19 patients. The virus might gain entry through the olfactory bulb and invade various parts of the brain, including the brainstem. Alternatively, the entry might also occur from peripheral circulation into the central nervous system by compromising the blood–brain barrier. Finally, yet another possible entry route could be its dispersal from the lungs into the vagus nerve via the pulmonary stretch receptors, eventually reaching the brainstem. Therefore, screening neurological symptoms in COVID‐19 patients, especially toward the breakdown of the respiratory center in the brainstem, might help us better understand this disease.

Background: The central nervous system (CNS) known to regulate the physiological conditions of human body, also itself gets dynamically regulated by both the physiological as well as pathological conditions of the body. These conditions get changed quite often, and often involve changes introduced into the gut microbiota which, as studies are revealing, directly modulate the CNS via a crosstalk. This cross-talk between the gut microbiota and CNS, i.e., the gut-brain axis (GBA), plays a major role in the pathogenesis of many neurodegenerative disorders such as Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and Huntington’s disease (HD). Objective: We aim to discuss how gut microbiota, through GBA, regulate neurodegenerative disorders such as PD, AD, ALS, MS and HD. Methods: In this review, we have discussed the present understanding of the role played by the gut microbiota in neurodegenerative disorders and emphasized the probable therapeutic approaches being explored to treat them. Results: In the first part, we introduce the GBA and its relevance, followed by the changes occurring in the GBA during neurodegenerative disorders and then further discuss its role in the pathogenesis of these diseases. Finally, we discuss its applications in possible therapeutics of these diseases and the current research improvements being made to better investigate this interaction. Conclusion: We concluded that alterations in the intestinal microbiota modulate various activities that could potentially lead to CNS disorders through interactions via the GBA.

New neurons were shown to born throughout adulthood, a process known as neurogenesis. Last year, the human hippocampal neurogenesis field was flipped on its head by a paper in Nature from Sorrells et al. questioning the presence of human hippocampal neurogenesis during adulthood (Nature2018555377381). Now, a new study by Moreno-Jiménez et al. reported that human brain can make new neurons well beyond middle age until the tenth decade of their life, and earlier studies have failed to find the neurogenesis due to its flawed methods. This paper also finds that production of new neurons drastically drops in patients suffering from Alzheimer’s disease. Here, we discuss key findings of this paper, emphasizing how improved protocols and tissue preservation lead to visualization of adult neurogenesis and further highlighting in what way this drop of neurogenesis in Alzheimer's disease brain could possibly open new roads to therapy.