Vanadium is a hard, silver-grey transition metal found in at least 60 minerals and fossil fuel deposits. Its oxide and other vanadium salts are toxic to humans, but the toxic effects depend on the vanadium form, dose, exposure duration, and route of intoxication. Vanadium is used by some life forms as an active center in enzymes, such as the vanadium bromoperoxidase of ocean algae and nitrogenases of bacteria. The structure and biochemistry of vanadate resemble those of phosphate, hence vanadate can be regarded as a phosphate competitor in a variety of biochemical enzymes such as kinases and phosphatases. In this review, we describe the biochemical pathways regulated by vanadium compounds and their potential therapeutic benefits for a range of disorders including type 2 diabetes, cancer, cardiovascular disease, and microbial pathology.

Neurological disorders are the major cause of disability, leading to a decrease in quality of life by impairing cognitive, sensorimotor, and motor functioning. Several factors have been proposed in the pathogenesis of neurobehavioral changes, including nutritional, environmental, and genetic predisposition. Vitamin D (VD) is an environmental and nutritional factor that is widely distributed in the central nervous system's subcortical grey matter, neurons of the substantia nigra, hippocampus, thalamus, and hypothalamus. It is implicated in the regulation of several brain functions by preserving neuronal structures. It is a hormone rather than a nutritional vitamin that exerts a regulatory role in the pathophysiology of several neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and multiple sclerosis. A growing body of epidemiological evidence suggests that VD is critical in neuronal development and shows neuroprotective effects by influencing the production and release of neurotrophins, antioxidants, immunomodulatory, regulation of intracellular calcium balance, and direct effect on the growth and differentiation of nerve cells. This review provides up-to-date and comprehensive information on vitamin D deficiency, risk factors, and clinical and preclinical evidence on its relationship with neurological disorders. Furthermore, this review provides mechanistic insight into the implications of vitamin D and its deficiency on the pathogenesis of neurological disorders. Thus, an understanding of the crucial role of vitamin D in the neurobiology of neurodegenerative disorders can assist in the better management of vitamin D-deficient individuals.

Chemotherapeutic agents such as doxorubicin, cyclophosphamide, fluorouracil, and cisplatin are commonly used to treat a variety of cancers and often result in chemobrain, which manifests as difficulties in learning and memory processes that can persist in the years following treatment. The current study aims to evaluate the cognitive function following treatment with these agents and the underlying mechanisms using a rat model of neuroinflammation and possible implication of thyroid toxicity in chemotherapy induced cognitive dysfunction. Wistar female rats were treated with a single dose of doxorubicin (DOX, 25 mg/kg), 5-fluorouracil (5-FU, 100 mg/kg), cisplatin (8 mg/kg), and cyclophosphamide (CYP, 200 mg/kg) by intraperitoneal injection. The cognitive performance of rats was then evaluated in spatial memory tasks using the Y-maze, novel object recognition (NOR), and elevated plus maze (EPM) tests. Serum levels of thyroid hormones (T3, T4, FT3, and FT4) and thyroid stimulating hormone (TSH) were measured, followed by estimation of TNFα, IL-6, and IL-1β in the hippocampal tissue. Results revealed that all the chemotherapeutic agents produced impairment of cognitive function, and significant increase of pro-inflammatory cytokines such as TNFα, IL-6 and IL-1β in the hippocampal tissues. There was a significant reduction in thyroid hormones (T3, FT3, and T4) and an increase in thyroid stimulating hormone (TSH) in serum, which may also have contributed to the decline in cognitive function. In conclusion, DOX, 5-FU, CYP, and cisplatin produces impairment of spatial memory possibly by inflammation of hippocampal neurons and endocrine disruption (hypothyroidism) in rats.

Herbal medicine, particularly in developing regions, remains highly popular due to its cost-effectiveness, accessibility, and minimal risk of adverse effects. Curcuma longa L., commonly known as turmeric, exemplifies such herbal remedies with its extensive history of culinary and medicinal applications across Asia for thousands of years. Traditionally utilized as a dye, flavoring, and in cultural rituals, turmeric has also been employed to treat a spectrum of medical conditions, including inflammatory, bacterial, and fungal infections, jaundice, tumors, and ulcers. Building on this longstanding use, contemporary biochemical and clinical research has identified curcumin—the primary active compound in turmeric—as possessing significant therapeutic potential. This review hypothesizes that curcumin’s antioxidant properties are pivotal in preventing and treating chronic inflammatory diseases, which are often precursors to more severe conditions, such as cancer, and neurological disorders, like Parkinson’s and Alzheimer’s disease. Additionally, while curcumin demonstrates a favorable safety profile, its anticoagulant effects warrant cautious application. This article synthesizes recent studies to elucidate the molecular mechanisms underlying curcumin’s actions and evaluates its therapeutic efficacy in various human illnesses, including cancer, inflammatory bowel disease, osteoarthritis, atherosclerosis, peptic ulcers, COVID-19, psoriasis, vitiligo, and depression. By integrating diverse research findings, this review aims to provide a comprehensive perspective on curcumin’s role in modern medicine and its potential as a multifaceted therapeutic agent.

Psychedelics such as lysergic acid diethylamide (LSD), psilocybin (magic mushrooms), and mescaline exhibit intense effects on the human brain and behaviour. In recent years, there has been a surge in studies investigating these drugs because clinical studies have shown that these once banned drugs are well tolerated and efficacious in medically supervised low doses called microdosing. Psychedelics have demonstrated efficacy in treating neuropsychiatric maladies such as difficult to treat anxiety, depression, mood disorders, obsessive compulsive disorders, suicidal ideation, posttraumatic stress disorder, and also in treating substance use disorders. The primary mode of action of psychedelics is activation of serotonin 5-HT_2A receptors affecting cognition and brain connectivity through the modulation of several downstream signalling pathways via complex molecular mechanisms. Some atypical antipsychotic drugs (APDs) primarily exhibit pharmacological actions through 5-HT_2A receptors, which are also the target of psychedelic drugs. Psychedelic drugs including the newer second generation along with the glutamatergic APDs are thought to mediate pharmacological actions through a common pathway, i.e., a complex serotonin–glutamate receptor interaction in cortical neurons of pyramidal origin. Furthermore, psychedelic drugs have been reported to act via a complex interplay between 5HT_2A, mGlu2/3, and NMDA receptors to mediate neurobehavioral and pharmacological actions. Findings from recent studies have suggested that serotoninergic and glutamatergic neurotransmissions are very closely connected in producing pharmacological responses to psychedelics and antipsychotic medication. Emerging hypotheses suggest that psychedelics work through brain resetting mechanisms. Hence, there is a need to dig deeply into psychedelic neurobiology to uncover how psychedelics could best be used as scientific tools to benefit psychiatric disorders including schizophrenia.

Garlic (Allium sativum L.) has served as a food source and medicinal agent for over thousands of years. Bioactive constituents, including allicin, diallyl sulfide/disulfide/trisulfide, ajoene, and S-allyl-cysteine, demonstrate antioxidant, anti-inflammatory, antithrombotic, antineoplastic, antimicrobial and neuroprotective properties. Convergent mechanistic evidence suggests the modulation of redox homeostasis, attenuation of pro-inflammatory signaling, regulation of platelet activation, and induction of apoptosis and cell-cycle arrest in tumor models. Computational studies, in conjunction with wet-lab data, offer molecular-level insights and guide candidate prioritization. Density functional theory elucidates radical-scavenging pathways and electronic descriptors that account for redox activity. Structure-based methods, including docking, molecular dynamics, and MM-GBSA, elucidate potential interactions between organosulfur scaffolds and enzymes or receptors pertinent to pharmacological effects. In silico ADME/Tox platforms predict generally favorable oral absorption for hydrophobic allyl sulfides, while polar derivatives exhibit more limited brain penetration. Emerging AI/ML pipelines combine network pharmacology with QSAR to focus on important targets and chemical types, while also spotting potential development. Formulation strategies, including nanoencapsulation and controlled-release systems, are utilized to stabilize labile thiosulfinates and modulate hydrogen-sulfide-releasing profiles, with potential applications in various disease conditions. Significant challenges encompass the standardization of preparations, variability in pharmacokinetics, heterogeneity in dose–response relationships, and interactions between drugs and nutrients or other drugs. The integration of mechanistic, computational, and formulation insights delineates a systematic approach to progress garlic-derived agents from diverse natural products to reproducible, mechanism-guided pharmaceuticals.