The bidirectional relationship between epilepsy and depression illustrates shared neurobiological mechanisms of neuroinflammation, hypothalamic–pituitary–adrenal axis dysregulation, and glutamatergic dysfunction. Depression is present in 20–55% of people with epilepsy, far greater than in the general population, while depression doubles epilepsy risk 2.5-fold, indicating shared pathophysiology. Neuroinflammatory mediators (interleukin-6, tumor necrosis factor alpha, high-mobility group box 1) establish a vicious cycle: seizures exacerbate inflammation and mood disruption, and stress lowers seizure thresholds. Hippocampal damage and cortisol toxicity also link these disorders, with early life stress imprinting lifelong risk via epigenetic alteration. Genetic studies identify pleiotropic genes (brain-derived neurotrophic factor) that regulate synaptic plasticity, serotonin activity, and immune responses. New treatments target shared pathways: ketamine and AMPAkines normalize glutamate tone; mGluR5 antagonists attenuate hyperexcitability and inflammation; DNA methyltransferase inhibitors reverse aberrant DNA methylation; and probiotics manipulate the gut–brain axis by boosting neuroprotective metabolites like butyrate. Despite challenges—transient effects, precision dosing, and blood–brain barrier penetration—these advances constitute a paradigm shift toward mechanistic repair rather than symptom management. The way forward includes clustered regularly interspaced short palindromic repeats (CRISPR)-based epigenome editing, biomarker-led therapies, and combination approaches (e.g., ketamine and probiotics). Such comorbidity needs to be managed holistically through integrated neuropsychiatry care, offering hope to patients with treatment-refractory symptoms.

Alopecia is a concerning dermatological issue and is also known as alopecia. This disease can affect men and women, influencing their confidence and appearance. It targets the scalp or any area of the entire body. Alopecia has become widespread worldwide over the years and has many types and different causes: hereditary, hormonal, immunological, therapeutic, or psychological. This review will present a comprehensive study of the physiological structure of hair and the different growth and shedding phases. It discusses using nano-drug delivery systems that contain natural substances of plant origin, which are effective, less harmful compared to current treatments, and help avoid adverse effects. This review also covers the latest trends in treating alopecia, including drug delivery systems, the materials and methods used to prepare these systems, three-dimensional (3D) bioprinting strategies, and plant extracts that may be utilized for treatment in the coming years.

This review explores the therapeutic potential of Allium cepa (onion) and Allium sativum (garlic), focusing specifically on their antidiabetic, cardioprotective, and antibacterial effects. These widely used medicinal plants are rich in bioactive compounds that contribute to their broad spectrum of pharmacological activities. Based on over two decades of scientific literature, this review synthesizes findings from more than 20 years of research to highlight the efficacy of these plant extracts. Rising chronic disease rates and antimicrobial resistance have renewed interest in plant-derived therapies; in the UAE context, Allium cepa and Allium sativum are promising candidates for integrative, sustainable interventions. This review further elucidates the mechanisms through which those bioactive constituents exert therapeutic effects, current extraction strategies, and challenges in enhancing formulations for functional health applications. Additionally, it addresses their role in sustainable healthcare practices due to their renewable nature and minimal environmental impact compared to synthetic pharmaceuticals.

The high comorbidity between autism spectrum disorder (ASD) and major depressive disorder (MDD) represents a complex and heterogeneous clinical challenge. Although elevated rates of depression in autistic individuals are well documented, the neurobiological and psychosocial mechanisms underlying this overlap remain debated, particularly in adulthood. This review synthesizes convergent evidence from genetics, monoaminergic and glutamatergic neurotransmission, neuroinflammatory signaling, hypothalamic–pituitary–adrenal axis dysregulation, large-scale brain network alterations, and gut–brain axis modulation to clarify the biological and psychosocial pathways contributing to ASD–depression comorbidity. In addition to shared neurobiological vulnerability, cumulative environmental stressors such as chronic social masking, stigma, and structural barriers may amplify depressive risk across the lifespan. We propose a hypothesis-generating framework that integrates these findings into a mechanistic stratification model, linking dominant biological profiles to targeted therapeutic hypotheses. Within this preliminary model, plant-derived compounds and microbiota-targeted interventions are hypothesized to serve as promising adjunctive strategies, particularly in neuroinflammatory and stress-related subtypes, complementing established pharmacological and neuromodulatory treatments. By moving beyond descriptive overlap toward biologically informed stratification, this review aims to support precision-guided and neurodiversity-affirming approaches for the assessment and treatment of depression in autistic individuals, especially adults who bear a disproportionate burden of mood disorders. This narrative review is based on a structured literature search conducted in PubMed, Scopus, and Web of Science using combinations of keywords such as “autism spectrum disorder,” “major depressive disorder,” “neuroinflammation,” and “gut–brain axis.