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The COVID-19 pandemic generated, in addition to severe symptoms, hospitalizations and deaths worldwide, as well as stress from the fear of the disease and social uncertainties, from restriction measures and social isolation. Stress from social isolation impacts mental health, aggravating existing conditions and triggering neuropsychiatric symptoms in individuals with biopsychosocial vulnerability. During and immediately after the period of social restriction imposed by the pandemic, the scientific community carried out several research protocols. These revealed results that relevantly demonstrate the harmful effect of the stress induced by the pandemic situation. This narrative review reports and discusses research results demonstrating impairments in psychiatric disorders such as autism spectrum disorder, dementia, eating disorders, schizophrenia, anxiety, and depression. In this sense, the community has identified a significant negative influence of social isolation on the mental health of individuals through the modification of individual routines and the absence of social interactions. Moreover, the community identified perceived differences related to the impacts on men and women. In addition to studies showing the effect of social isolation on disorders, an evaluation of protocols with some possible therapeutic intervention strategies during times of social restriction was developed. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) is a prevalent psychiatric disorder that has damage to people's quality of life. Tryptophan is the precursor to serotonin, a critical neurotransmitter in mood modulation. In mammals, most free tryptophan is degraded by the kynurenine pathway (KP), resulting in a range of metabolites involved in inflammation, immune response, and neurotransmission. The imbalance between quinolinic acid (QA), a toxic metabolite, and kynurenic acid (KynA), a protective metabolite, is a relevant phenomenon involved in the pathophysiology of MDD. Proinflammatory cytokines increase the activity of the enzyme indoleamine 2,3-dioxygenase (IDO), leading to the degradation of tryptophan in the KP and an increase in the release of QA. IDO activates proinflammatory genes, potentiating neuroinflammation and deregulating other physiological mechanisms related to chronic stress and MDD. This review highlights the physiological mechanisms involved with stress and MDD, which are underlying an imbalance of the KP and discuss potential therapeutic targets., (© 2024 Walter de Gruyter GmbH, Berlin/Boston.)

Dementia is an umbrella term for a broad group of age-associated neurodegenerative diseases. It is estimated that dementia affects 50 million people worldwide and that Alzheimer's disease (AD) is responsible for up to 75% of cases. Small extracellular senile plaques composed of filamentous aggregates of amyloid β (Aβ) protein tend to bind to neuronal receptors, affecting cholinergic, serotonergic, dopaminergic and noradrenergic neurotransmission, leading to neuroinflammation, among other pathophysiologic processes and subsequent neuronal death, followed by dementia. The amyloid cascade hypothesis points to a pathological process in the cleavage of the amyloid precursor protein (APP), resulting in pathological Aβ. There is a close relationship between the pathologies that lead to dementia and depression. It is estimated that depression is prevalent in up to 90% of individuals diagnosed with Parkinson's disease, with varying severity, and in 20 to 30% of cases of Alzheimer's disease. The hypothalamic pituitary adrenal (HPA) axis is the great intermediary between the pathophysiological mechanisms in neurodegenerative diseases and depression. This review discusses the role of Aβ protein in the pathophysiological mechanisms of dementia and depression, considering the HPA axis, neuroinflammation, oxidative stress, signalling pathways and neurotransmission., (© 2024 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society). Published by John Wiley & Sons Ltd.)

Anxiety and depression are prevalent mental disorders around the world. The etiology of both diseases is multifactorial, involving biological and psychological issues. The COVID-19 pandemic settled in 2020 and culminated in several changes in the routine of individuals around the world, affecting mental health. People infected with COVID-19 are at greater risk of developing anxiety and depression, and individuals previously affected by these disorders have worsened the condition. In addition, individuals diagnosed with anxiety or depression before being affected by COVID-19 developed the severe illness at higher rates than individuals without mental disorders. This harmful cycle involves several mechanisms, including systemic hyper-inflammation and neuroinflammation. Furthermore, the context of the pandemic and some previous psychosocial factors can aggravate or trigger anxiety and depression. Disorders are also risks for a more severe picture of COVID-19. This review discusses research on a scientific basis, which brings evidence on biopsychosocial factors from COVID-19 and the context of the pandemic involved in anxiety and depression disorders., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Major depressive disorder (MDD) is one of the most prevalent disorders and causes severe damage to people's quality of life. Lifelong stress is one of the major villains in triggering MDD. Studies have shown that both stress and MDD, especially the more severe conditions of the disorder, are associated with inflammation and neuroinflammation and the relationship to an imbalance in tryptophan metabolism towards the kynurenine pathway (KP) through the enzymes indoleamine-2,3-dioxygenase (IDO), which is mainly stimulated by pro-inflammatory cytokines and tryptophan-2,3-dioxygenase (TDO) which is activated primarily by glucocorticoids. Considering that several pathophysiological mechanisms of MDD underlie or interact with biological processes from KP metabolites, this chapter addresses and discusses the function of these mechanisms. Activities triggered by stress and the hypothalamic-pituitary-adrenal (HPA) axis and immune and inflammatory processes, in addition to epigenetic phenomena and the gut-brain axis (GBA), are addressed. Finally, studies on the function and mechanisms of physical exercise in the KP metabolism and MDD are pointed out and discussed., (© 2023. The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd.)