Aim: Neuroinflammation is a characteristic of multiple sclerosis (MS). Resveratrol (RSV) has potent antioxidant properties and has emerged as a promising therapeutic agent for various inflammatory diseases. This study investigated the effects of RSV on inflammatory responses via reactive oxygen species (ROS) production and leukocyte cytokine secretion in patients with MS and healthy controls.

Methods: The effects of RSV on ROS production in resting and stimulated granulocytes (in the presence of opsonized particles) were assessed using luminol-dependent chemiluminescence. The cytokines interleukin (IL)-10, IL-1β, IL-6, and high mobility group box 1 (HMGB1) in the supernatant of peripheral blood mononuclear cells (PBMNCs) were quantified using enzyme-linked immunosorbent assay (ELISA).

Results: RSV significantly downregulated ROS production in resting and stimulated granulocytes in patients with MS and healthy controls. In the control group, RSV reduced IL-6 levels by 49% in the PBMNC supernatant, whereas IL-6 levels remained unchanged in the MS group. Interestingly, higher levels of IL-10 were detected in PBMNC supernatants from patients with MS than in controls. No significant changes were observed in IL-1β and HMGB1 levels in the PBMNC supernatant.

Conclusions: Controlling ROS production is a key target for treating inflammatory diseases. Our findings suggest that RSV can effectively modulate ROS production in MS, highlighting its potential as a promising adjunct therapy for controlling oxidative innate immune responses in MS.

Cognitive impairment is a common age-related comorbidity with blood-brain barrier (BBB) leakage a key event. BBB leakage increases with age, but the mechanisms are still not completely understood. In the current article, we briefly discussed the role of neutrophil extracellular traps (NETs) in age-associated increase in cognitive impairment. NETosis is a process neutrophils release web-like structures called NETs composed of DNA, histones, and antimicrobial proteins. These NETs act as physical barriers to trap and kill pathogens, such as bacteria, viruses, and fungi. Excessive NETs formation has been associated with various pathological conditions such as thrombosis, cancer metastasis, inflammatory diseases, and autoimmune disorders. Recent studies further indicated that NETosis plays a key role in the BBB leakage during stroke and depletion of neutrophils can attenuate the pathology of Alzheimer’s disease (AD) in murine models. In the current article, we briefly discussed the putative role of NETosis in BBB leakage and age-related cognitive impairment. It should briefly summarize the main content of the article, and it may include the background, purpose, significance, methods and conclusions of the article.

As an integral part of human chronobiology, the circadian system plays a crucial role in regulating key biological functions, including sleep and the intricate hormonal rhythms of melatonin (MLT) and cortisol (CORT). Scholars have increasingly recognized environmental stressors as significant contributors to disturbed sleep patterns. Albeit vigorously discussed individually, the literature lacks comprehensive insights into the synergistic effect of artificial light at night (ALAN) and noise. The aim of this review is to look into the intricate interplay of the ALAN effects on sleep architecture, the modulation of circadian function, and how this influences homeostatic sleep. Furthermore, ALAN suppresses MLT secretion, which is most pronounced in response to short wavelengths of light. In addition, this review will demonstrate how exposure to noise during sleep elevates CORT and noradrenaline levels, which contributes to stress-related diseases and sleep disturbances. ALAN and noise, persistently emitted into the environment, share intrinsic mechanisms with comparable characteristics. Therefore, understanding their combined impact has become increasingly urgent. Pre-sleep exposure to both ALAN and noise acts as a potent stressor, with the potential to disrupt sleep patterns. Interestingly, during sleep, noise emerges as the predominant influence on sleep quality. Moreover, these stressors often synergize and amplify one another’s adverse effects. Thus, limiting their exposure is crucial for cultivating a sustainable environment conducive to quality sleep and overall well-being.

Chronic neuropathic pain is a significant public health issue affecting an estimated 1.5 billion individuals worldwide. The mechanisms underlying chronic pain are multifaceted and not fully understood. Chronic pain amplifies specific neural pathways through peripheral and central sensitization triggered by repeated exposure to noxious stimuli, ultimately resulting in physical and emotional pain. Traditional treatment options targeting these mechanisms, such as opioid and non-opioid analgesics, are associated with adverse effects, addiction, and suboptimal pain relief. Using psychedelics to treat chronic pain is an area of growing interest. While psychedelic substances, such as psilocybin, lysergic acid diethylamide, mescaline, and 3,4-methylenedioxymethamphetamine are primarily associated with recreational use or spiritual practices, emerging evidence suggests their potential therapeutic benefits for various mental health disorders, including chronic pain. Psychedelics alter pain perception by directly activating serotonin receptors, exerting anti-inflammatory effects, enhancing descending inhibition, opening a window of neuroplasticity, and facilitating synaptic remodeling. This review mainly elucidates the ongoing research regarding the psychedelic mechanisms of action, pharmacology, clinical applications, and therapeutic potential in treating neuropathic pain.

The overt expression of circadian rhythms is a manifestation of the suprachiasmatic nucleus (SCN). This integrated complex function based on the transcriptional/translational feedback loops (TFFLs), neurotransmitters, genes, networking, and synchronization is essential for this molecular mechanism to operate effectively. Neurotransmitters by participating in the entrainment to the environmental light conditions and synchronization contribute to the robustness of the rhythm. Neurotransmitter signaling is the hallmark of circadian rhythm expression. Even during development, neuropeptides contribute to the dramatic cellular, genetic, and network circuit changes. Participating neurotransmitters are seen in afferent inputs, efferent output, and the SCN. There are numerous neurotransmitters involved in SCN function. Astrocytes co-exist with neurons in the SCN. Autonomous clocks seen in astrocytes can drive circadian behavior like neurons. Astrocytes and neurons are acting as two arms of the clock. Coupling through glutamate released from astrocytes gives additional evidence for the role of astrocytes. Glutaminergic signaling from astrocytes may also be responsible for timekeeping. The neurotransmitters can independently and in combination execute the functions making SCN a unique pacemaker for the overt expression of circadian rhythms. This reassessment also highlights its role in underlying molecular mechanisms, genetic linkage, and the recently known role of astrocytes.

Epilepsy, a neurological disorder characterized by recurrent seizures, presents a complex interplay of cellular and molecular mechanisms. The symptoms manifest themselves at various scales, from ion channels to brain regions to behavior in humans. Various screening, treatment, and preventive measures use this knowledge to tackle the disorder effectively. This article aims to summarize the current state of the art in epileptic markers from ion channels, astrocytes, and synaptic imbalance to whole brain Network Dynamics. Recent research has shed light on the critical involvement of astrocytes, the multifunctional glial cells, in the pathogenesis and modulation of epileptic seizures in humans. Astrocytes, once considered as mere supportive cells, are now recognized as active participants in the regulation of neuronal excitability, synaptic transmission, and brain homeostasis. Ion channel imbalance is one of the widely studied areas in the context of epilepsy and is partially addressed in the abstract. Recent advances in computational neuroscience have led to the development of whole brain network models, providing valuable tools for studying the complex dynamics of epileptic seizures. These models integrate diverse biological factors, including neuronal connectivity, synaptic dynamics, and cellular properties, to simulate the spatiotemporal patterns of epileptic activity across brain regions. Through computational simulations and analysis, whole brain network models offer insights into seizure initiation, propagation, and termination mechanisms, shedding light on the dynamic interactions between epileptic foci and distributed brain networks. Moreover, these models facilitate the exploration of network-based biomarkers for seizure prediction and intervention optimization. Challenges and limitations, such as model complexity and validation against experimental data, are also discussed. Despite these challenges, whole brain network models represent a promising approach for advancing our understanding of epilepsy and identifying novel therapeutic strategies. Future research efforts should focus on refining model fidelity, incorporating multimodal data, and translating computational findings into clinically relevant applications, ultimately improving the management and treatment of epilepsy patients.