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.

Chronic stress is linked to a variety of neuropsychiatric ailments, many of which are characterized by cognitional alterations. Stress animal models showed equivalent behavioural alterations, including working memory and cognitive flexibility impairment. It's consistent with morphological alterations in the hippocampus and frontal cortex, all of which play important roles in controlling these behaviours. Growing evidence suggests that changes in autophagy could be contributing to the disorders observed in neuropsychiatric diseases. Chronic stress can affect autophagy signaling in the hippocampus and frontal cortex; besides, this is believed to be related to changes in neuronal morphology. Recently, animal models have explained the function of autophagy signaling in behavioural changes caused by stress. Together, the findings indicate that autophagy plays an essential role in mediating cognitive impairment seen in the presence of stress. Increasing our knowledge of the effects of stress on AMPK/mTOR autophagic signaling will eventually support the discovery of more effective medications for people suffering from cognitive impairment.Copyright © 20xx by the authors. This article is an open access article distributed under the terms and conditions Creative Commons Attribution-Share Alike 4.0 International Public License (CC BY-SA 4.0)

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.

Ulcerative colitis (UC) is a refractory inflammatory bowel disease with ongoing colonic inflammation and extra-intestinal manifestations, including cognitive impairment. In this study, we evaluated the peripheral and central effects of clemastine on cognitive impairment induced by UC using an acetic acid (1 ml, 4% v/v) model with emphasis on the role of PI3K/Akt/GSK-3β signaling, ferroptosis, and autophagy in its possible mediated neuroprotection. Clemastine revealed a dose-dependent improvement of colonic damage linked with UC, as demonstrated by inhibition of TNF-α, IL-1β, and caspase-3 levels along with upregulation of claudin-1 expression. Importantly, the preservation of gut membrane integrity was associated with amelioration of UC-induced systemic inflammation together with restoration of PI3K/Akt/GSK-3β signaling in the brain. Additionally, the neuroprotective actions of clemastine included the prevention of neuronal injury and death as evidenced by inhibition of oxidative stress markers and microglial activation (Iba-1 expression), which could exacerbate the neuroinflammatory response. Concurrently, inhibition of the pathological autophagic dysfunction and ferroptosis profile by clemastine, as clarified by LC3-II downregulation and LC3-I and GPX4 upregulation, led to behavioral and cognitive improvements, which were proven by decreased levels of Aβ and tau protein. Importantly, by crossing the BBB, clemastine could exert additional anti-inflammatory and neuroprotective effects by affecting the central assessed pathways. In conclusion, these findings clarify the pivotal role of clemastine in the management of colonic inflammation-associated cognitive decline through modulating multiple and interacting peripheral and central pathways to provide its potent neuroprotection.