Stroke is a neurological condition characterized by blood vessel obstruction, leading to localized loss of brain function and associated neurological manifestations. Fatal cases of stroke are underrepresented in case-control studies compared to incident cases attributed to common causes. Hemorrhagic and ischemic strokes make up the primary classifications of stroke. This review describes the most recent findings on stem cells and how they can be used to treat stroke in people with serious illnesses. It highlights the potential of stem cells in stroke rehabilitation and gives an overview of their various forms and mechanisms of action. Stem cells promote stroke recovery through diverse pathways, depending on the cell type employed. Recent advancements in cell therapy for stroke include different stem cell sources, application methods, modification of culturing media and stem cells ex vivo, stem cell-derived extracellular vesicles, and 3D bioprocessing methods. Pre-clinical and clinical trials are important in assessing the effectiveness of the therapy, as the effect varies among individuals. Data were collected from different trials, highlighting the need for further advancements in stem cell therapy to improve its outcomes for treating stroke.

The emergence of artificial intelligence (AI) has revolutionized the landscape of epilepsy education and management by providing innovative solutions to the challenges of diagnosis, treatment, and patient care. This review evaluates the multifaceted role of AI in epilepsy, focusing on its impact on early diagnosis, seizure prediction, and the development of personalized treatment plans. AI tools, including machine learning algorithms and neural networks, have demonstrated significant promise in enhancing diagnostic accuracy and identifying epileptic patterns. This study explores various AI-driven educational platforms designed to improve the knowledge and skills of healthcare professionals, patients, and caregivers in managing epilepsy. Moreover, AI applications in wearable devices and mobile health platforms facilitate real-time monitoring and patient engagement, ultimately improving quality of life. However, integrating AI into clinical practice presents several challenges, including the need for large and high-quality datasets, interdisciplinary collaboration, data privacy, and ethical considerations. This review highlights these barriers while suggesting uniform protocols and frameworks for efficiently translating AI technologies into clinical practice. It underscores AI’s transformative potential in epilepsy care and education, advocating for ongoing research and collaborative efforts among technologists, clinicians, and educators, while emphasizing the importance of user-friendly design, regular assessments, and ethical considerations to maximize AI’s impact in this critical field.

Major depressive disorder is a complex neurological condition marked by persistent sadness, hopelessness, and loss of interest in daily activities for at least 2 weeks. It significantly affects mental, emotional, and physical health and is a major contributor to global disease. In India, rising depression rates have demonstrated the necessity of better understanding its causes for improved interventions and public health policies. This review comprehensively explores the diverse factors contributing to the increasing prevalence of depression in India. An unstructured survey of research articles and a detailed literature review were conducted using electronic databases, including Google Scholar, PubMed, Springer, and Elsevier. The findings reveal that in India, depression stems from a combination of external and internal risk factors. External factors such as cultural norms and gender roles heavily influence societal perceptions of mental health and individual psychological experiences. Other significant external contributors include educational stress, unemployment, occupational pressure, and challenges from rapid urbanization. Meanwhile, internal factors including genetic predisposition and epigenetic mechanisms play a critical role in individual susceptibility to depression. These biological factors interact with environmental stressors to shape the onset and progression of depression. Based on the findings, rising depression rates in India necessitate targeted efforts to address modifiable factors, such as stigma, work stress, and mental healthcare access, while recognizing genetic influences. A comprehensive strategy that integrates policy reforms and community initiatives is crucial for reducing the burden of depression in India.

Olfactory dysfunction is observed in over 95% of patients with Parkinson’s disease (PD). This study examines the relationship between gray matter volume (GMV) and olfactory impairment in a cohort of 182 subjects, including PD patients and healthy controls (HCs). Using the Iran Smell Identification Test, which is a standardized 24-item olfactory identification assessment, to evaluate the olfactory performance, PD patients were divided into two groups (scores ranging from 0 to 18 indicate olfactory dysfunction, while scores from 19 to 24 indicate normal olfaction): those with normal smell (PD-NS, n = 23) and those with smell disorders (PD-SD, n = 69). Differences in GMV were analyzed using voxel-based morphometry. Statistical analysis was conducted using SPSS 26. The results revealed that the PD-NS group exhibited reduced GMV in the right thalamus and the left parahippocampal gyrus compared to the HCs. Furthermore, the HC group demonstrated no statistically significant olfactory dysfunction. In contrast, the PD-SD group showed significant decreases in GMV in the right entorhinal cortex and both the right and left hippocampus compared to both the HC and PD-NS groups. These findings indicate that PD patients experience more severe olfactory dysfunction in hippocampal regions than the HC group, likely attributed to the initial pathological loss of gray matter in both the right and left hippocampus.

Globally, traumatic brain injury (TBI) is one of the major causes of morbidity and mortality, with increased incidence reported among veterans. In this study, we explored the relationship between TBI and subsequent screening of depressive symptoms, with further analysis stratified by veteran status. For this study, the National Health Interview Survey data for 2023 was used, which was conducted among 29,522 non-institutionalized U.S. adults aged 18 and older. The patient health questionnaire-2 was used to screen for depression. Self-reported incidence of lifetime TBI was documented. From a Chi-square test, a significant association was observed between TBI and depression (p<0.05), with TBI more commonly being reported among veterans compared to non-veterans. Our regression model indicated that, when adjusted for sociodemographic and health variables, TBI was associated with 1.80 times higher odds of depression among the whole sample population (adjusted odds ratio [aOR] = 1.80; 95% confidence interval [CI] 1.61 - 2.02, p<0.05). When stratified by veteran status, veterans with TBI had 2.92 times higher odds of depression (aOR = 2.92; 95% CI 2.05 - 4.14, p<0.05). Compared to the whole general population, veterans with a brain injury history have higher odds of depression, identifying them as a key group in prioritizing depression management in the United States population.

Previous studies have reported the neuroprotective effects of exercise in epilepsy. Hence, this study aimed to investigate the potential mechanisms underlying these neuroprotective effects by examining changes in high-density lipoprotein (HDL), low-density lipoprotein (LDL), and Vitamin D levels. Wistar rats were divided into four groups: sham, pentylenetetrazole (PTZ), exercise (EX), and PTZ + EX. Seizures were induced in the PTZ and PTZ + EX groups through intraperitoneal administration of PTZ (35 mg/kg) every other day for 1 month. The EX and PTZ + EX groups underwent daily exercise sessions (30 min/session) for 1 month. Serum levels of Vitamin D, HDL, and LDL were measured, and neuronal damage was assessed in the hippocampus and somatosensory cortex. The PTZ + EX group showed a significant increase in serum HDL and Vitamin D levels compared to the PTZ group. Histological analysis revealed a significant increase in neuronal damage in the PTZ group compared to the sham group. In contrast, both PTZ + EX and EX groups demonstrated a reduction in neuronal damage compared to the PTZ group. These findings suggest that HDL and Vitamin D may contribute to the neuroprotective benefits of exercise. Furthermore, exercise could potentially serve as a complementary strategy to counteract Vitamin D and HDL deficiencies associated with long-term antiepileptic drug use.

Glioblastomas (GBMs) are highly aggressive and lethal primary brain tumors, known for their rapid proliferation, diffuse infiltration, and resistance to conventional therapies. Recent studies have highlighted the involvement of transient receptor potential melastatin 7 (TRPM7) in regulating GBM progression through its dual function as an ion channel and a serine/threonine protein kinase. TG100-115, initially characterized as a phosphoinositide 3-kinase γ/δ inhibitor, has recently been identified as a novel inhibitor of TRPM7 kinase. However, its potential pharmacological effects in GBM cells have not been fully elucidated. In this study, we investigated the anti-GBM effects of TG100-115 in U251 glioma cells. Cell viability and proliferation were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, whereas cell motility and invasiveness were determined through wound healing and transwell assays, respectively. Western blotting was used to detect the expression of key proteins involved in the apoptotic and molecular signaling pathways. Our findings revealed that TG100-115 significantly diminished the viability of U251 cells by promoting apoptosis while concurrently inhibiting the migratory and invasive activities of GBM cells. Mechanistically, TG100-115 enhanced apoptotic signaling by modulating B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, and cleaved caspase-3 levels. It also altered the phosphorylation status of protein kinase B and cofilin - both critical for cell survival and cytoskeletal dynamics. In conclusion, these findings suggest that TG100-115, by targeting TRPM7 kinase, exhibits promising therapeutic potential for GBM treatment and provides novel insights into targeting TRPM7-associated pathways in aggressive brain tumors.

Patients with Alzheimer’s disease and related dementia (ADRD) have a higher risk for comorbidities than non-cognitively impaired age-matched individuals. Because ADRD is an age-related disorder, it was hypothesized that younger patients with ADRD have a lower prevalence of comorbidities than their older counterparts. To test this hypothesis, the following four patient cohorts were defined in the TriNetX Analytics Network database based on the presence or absence of International Classification of Diseases, Tenth Revision (ICD-10) codes G30 (Alzheimer’s disease), and/or F01 (dementia in other diseases classified elsewhere) in their health care records who had health care visits from 2021 to 2023: individuals aged 65 - 80 years with and without ADRD diagnosis and individuals aged ≥90 years with and without ADRD diagnosis. Patients with ADRD in both age groups had a higher prevalence of comorbidities in almost all ICD-10 chapters than age-matched non-ADRD individuals. The younger ADRD cohort showed a comorbidity pattern that was significantly different than that of their age-matched cohort (p < 0.0001); however, it was not statistically different than the comorbidity pattern of the older ADRD cohort (p = 0.80). Similarly, the younger non-ADRD cohort showed a comorbidity pattern that was not statistically different than that of the older non-ADRD cohort (p = 0.28). These results indicated that ADRD diagnosis is associated with coincident multiorgan dysfunction in a pattern that is almost identical between the two different age groups. These data also suggested that cognitive impairment associated with ADRD is only a single component of a multiorgan senescence syndrome. Overall, this study revealed that optimizing the health care management of non-cognitive organ dysfunction in patients with ADRD may improve their overall health and, thereby, delay the progression of cognitive impairment.

Subcortical band heterotopia (SBH) is a developmental disorder in which neuroblasts migrating from the periventricular zone to the cortex cannot reach their final destination. Subcortical bands might interfere with axonal development. Therefore, this study examined white matter organization in 10 healthy controls and 2 patients with drug-resistant epilepsy (referred to as patients 1 and 2), in whom diagnostic magnetic resonance imaging revealed subcortical bands of gray matter. Diffusion tensor imaging, advanced tractography methods, and functional imaging were performed in patient 2. The number of subcortical fibers decreased significantly in both patients. The heterotopias interrupted the propagation of the tracking algorithm. Only a small number of tracts were generated from inside the heterotopias. According to the literature and our findings, SBHs appear to differ in their localization, extension, and structure. Some heterotopias might allow the propagation of tractography, thereby creating the impression that tracts are passing through, whereas others interrupt the propagation, as observed in our cases. In addition, a reduction in the number of subcortical white matter fibers was observed. These findings may have consequences in pre-surgical planning. The generalization of seizures might be facilitated by a non-reduction in SCWM fibers and tracts passing through the band, and these patients might benefit more from extensive resections of the epileptogenic zone than others.

Variants in the ryanodine receptor 2 (RYR2) gene are primarily associated with catecholaminergic polymorphic ventricular tachycardia. However, recent studies have also identified potential links to neurological pathologies, including Alzheimer’s disease, benign epilepsy of childhood, and neurodevelopmental disorders. Despite these findings, there is limited data on the association between RYR2 variants and additional neurological symptoms, such as autonomic dysfunction. This case report describes the clinical progression of a father-son pair, who carry a novel pAsn2517Ser variant in the RYR2 gene, identified through genetic studies. The report highlights distinct neurological manifestations in both individuals: the father exhibited Alzheimer’s-like cognitive dysfunction, while the son presented with an autonomic disorder. This case aims to provide additional information on the role of RyR2 in the brain and the symptomatology associated with pathological variants. Given that both father and son share the same RYR2 mutation, the observed neurological manifestations are likely attributable to this genetic alteration. These cases offer novel clinical insights into the role of cytoplasmic calcium regulators and their impact on the neurological system.