Background: In December 2019, Wuhan City in Hubei Province, China witnessed an outbreak of a novel type of coronavirus (COVID-19), named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The sharp rise in the number of infected cases and the surge spike in fatalities worldwide prompted the World Health Organization (WHO) to declare this rapid outbreak a global pandemic in March 2020. The economic, health, and social ramifications of COVID-19 induced fear and anxiety all over the world. Objective: The purpose of this review is to discuss how precautionary measures and restrictions imposed by governments, such as quarantines, lockdowns, and social distancing, have not only caused economic losses, but also a rise in mental health problems specifically post-traumatic stress disorder (PTSD). Methods: A deep comprehensive review of the relevant literature regarding the pandemic and its debilitating consequences on the psychological status of the public was performed. Results: This review illustrates that the pandemic had a traumatic impact on the psychological functioning of the public, particularly COVID-19 survivors, older adults, and healthcare workers, due to difficulties in coping with new realities and uncertainties. Conclusion: In this review, we have discussed the psychological implications of this pandemic and we have provided an extensive background for understanding options regarding PTSD management in healthy individuals and those with preexisting conditions.

The roles of the hypothalamus and particularly the lateral hypothalamus (LH) in the regulation of inflammation and pain have been widely studied. The LH consists of a parasympathetic area that has connections with all the major parts of the brain. It controls the autonomic nervous system (ANS), regulates feeding behavior and wakeful cycles, and is a part of the reward system. In addition, it contains different types of neurons, most importantly the orexin neurons. These neurons, though few in number, perform critical functions such as inhibiting pain transmission and interfering with the reward system, feeding behavior and the hypothalamic pituitary axis (HPA). Recent evidence has identified a new role for orexin neurons in the modulation of pain transmission associated with several inflammatory diseases, including rheumatoid arthritis and ulcerative colitis. Here, we review recent findings on the various physiological functions of the LH with special emphasis on the orexin/receptor system and its role in mediating inflammatory pain.

Rheumatoid arthritis (RA) is a chronic inflammatory and autoimmune disease characterized by the attack of the immune system on the body’s healthy joint lining and degeneration of articular structures. This disease involves an increased release of inflammatory mediators in the affected joint that sensitize sensory neurons and create a positive feedback loop to further enhance their release. Among these mediators, the cytokines and neuropeptides are responsible for the crippling pain and the persistent neurogenic inflammation associated with RA. More importantly, specific proteins released either centrally or peripherally have been shown to play opposing roles in the pathogenesis of this disease: an inflammatory role that mediates and increases the severity of inflammatory response and/or an anti-inflammatory and protective role that modulates the process of inflammation. In this review, we will shed light on the neuroimmune function of different members of the heat shock protein (HSPs) family and the complex manifold actions that they exert during the course of RA. Specifically, we will focus our discussion on the duality in the mechanism of action of Hsp27, Hsp60, Hsp70, and Hsp90.

Contrast agents administered daily led to gadolinium retention in rat central and peripheral nervous tissues; gadodiamide but not gadoterate meglumine led to pain hypersensitivity, but neither alte... Background Despite the wide use of gadolinium-based contrast agents (GBCAs) for enhanced MRI, their neurochemical and behavioral consequences, if any, remain poorly understood. Purpose To investiga...

Traumatic brain injury (TBI) represents a major health concern affecting the neuropsychological health; TBI is accompanied by drastic long-term adverse complications that can influence many aspects of the life of affected individuals. A substantial number of studies have shown that mood disorders, particularly depression, are the most frequent complications encountered in individuals with TBI. Post-traumatic depression (P-TD) is present in approximately 30% of individuals with TBI, with the majority of individuals experiencing symptoms of depression during the first year following head injury. To date, the mechanisms of P-TD are far from being fully understood, and effective treatments that completely halt this condition are still lacking. The aim of this review is to outline the current state of knowledge on the prevalence and risk factors of P-TD, to discuss the accompanying brain changes at the anatomical, molecular and functional levels, and to discuss current approaches used for the treatment of P-TD.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the progressive loss of neurons leading to cognitive and memory decay. The main signs of AD include the irregular extracellular accumulation of amyloid-beta (A beta) protein in the brain and the hyper-phosphorylation of tau protein inside neurons. Changes in A beta expression or aggregation are considered key factors in the pathophysiology of sporadic and early-onset AD and correlate with the cognitive decline seen in patients with AD. Despite decades of research, current approaches in the treatment of AD are only symptomatic in nature and are not effective in slowing or reversing the course of the disease. Encouragingly, recent evidence revealed that exposure to electromagnetic fields (EMF) can delay the development of AD and improve memory. This review paper discusses findings from in vitro and in vivo studies that investigate the link between EMF and AD at the cellular and behavioural level, and highlights the potential benefits of EMF as an innovative approach for the treatment of AD.