Karthikeyan Ramanujam

Patients with Autism Spectrum Disorder (ASD) may be particularly prone to develop COVID-19. An unusual extended course of COVID-19 disease illness has been reported in one ASD patient and a group of patients have COVID-19 disease in a neurodevelopmental facility. It has been widely reported that many of those with ASD have substantial sleep disorders with low levels of melatonin and various genetic alterations related to melatonin production have been found. Several lines of evidence point to a substantial role of melatonin in the body’s innate defense system including acting as a scavenger, an antioxidant and modulating the immune system. We therefore hypothesize that melatonin deficiency may predispose those ASD patients who have low melatonin output to COVID-19 disease. Potential implications for treatment are discussed.

It has been suggested that distress secondary to isolation and fear can exert a more negative effect in the long-term than COVID-19 infection itself. This narrative review aims to provide a global view on the neuropsychiatric consequences of COVID-19 that can be ascribed to a number of factors ranging from the direct effect of infection, to the body’s responses against infection or to the psychological sequelae of social isolation, unemployment, and fear for one’s health and livelihood. Findings show that, with respect to the infection itself, the more severe the respiratory infection, the more likely are central nervous system (CNS) complications. Immune reactions to the infection may result in symptoms similar to chronic fatigue as well as neurocognitive deficits which last long after the infection is over. An increase in symptoms of depression, anxiety, and trauma-related stress may also follow upon economic fears and isolation from friends and family. The consequences of the pandemic are not limited to adults. Children learning remotely and away from classmates and routine activities may develop adjustment disorders, acute stress disorder, and a variety of manifestations of grief. A summary of case reports suggests that COVID-19-related stress, economic recession, and political unrest increase the risk of suicidal behaviors and acts of violence. However, it is not known whether manifestations of mental disorders all result from social causes, or whether some may be caused by CNS complications. In conclusion, COVID-19 leaves in its wake neuropsychiatric symptoms that result from several interrelated causes. We recommend a comprehensive approach while dealing with neuropsychiatric symptoms during the pandemic that includes all disease models i.e., biological, psychosocial, and economic in the causation as well as management.

Sleep and the circadian clock are intertwined and have persisted throughout history. The suprachiasmatic nucleus (SCN) orchestrates sleep by controlling circadian (Process C) and homeostatic (Process S) activities. As a "hand" on the endogenous circadian clock, melatonin is critical for sleep regulation. Light serves as a cue for sleep/wake control by activating retino-recipient cells in the SCN and subsequently suppressing melatonin. Clock genes are the molecular timekeepers that keep the 24 h cycle in place. Two main sleep and behavioural disorder diagnostic manuals have now officially recognised the importance of these processes for human health and well-being. The body's ability to respond to daily demands with the least amount of effort is maximised by carefully timing and integrating all components of sleep and waking. In the brain, the organization of timing is essential for optimal brain physiology.

In recent years, there has been an increased prevalence of type 2 diabetes mellitus (T2DM) and depression across the world. This growing public health problem has produced an increasing socioeconomic burden to the populations of all affected countries. Despite an awareness by public health officials and medical researchers of the costs associated with these diseases, there still remain many aspects of how they develop that are not understood. In this article, we propose that the circadian clock could be a factor that coordinates both the neurobehavioral and metabolic processes that underlie depression and T2DM. We propose further that this perspective, one which emphasizes the regulatory effects of clock gene activity, may provide insights into how T2DM and depression interact with one another, and may thus open a new pathway for managing and treating these disorders.

A number of observations support the involvement of circadian clock genes in the regulation of metabolic processes. One of these circadian genes,Intravenous blood samples were collected to obtain white blood cells from 302 T2DM patients and 330 non-diabetic, age- and sex-matched, individuals.Frequency of five repeat allele was higher, and that of four repeat allele lower, in T2DM patients as compared to non-diabetic controls (χThe results indicate an association of