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Migraine is a widespread and debilitating disorder. Recent evidence suggests a role of seasonal and circadian rhythmicity in migraine episodes. We investigated the pattern of migraine attacks over 1 year in the North Indian population. A questionnaire was provided to 120 migraine patients at the end of each of the six seasons according to the Indian calendar. The frequency, pain intensity, and duration of migraine episodes were significantly higher during the hot summer (7.92 ± 0.70, 6.63 ± 0.17, and 8.73 ± 0.99, respectively) and monsoon (8.11 ± 0.72, 6.64 ± 0.17, and 8.00 ± 0.94, respectively) compared to the cold winter months. There was a gradual decrease from summer to winter, with 77.2% of patients reporting diurnal rhythmicity to their attacks, and 34.5% of patients reporting occurrences in the afternoons, increasing from colder to hotter months. Increased incidence during summer, monsoon, and afternoons should be considered in planning prophylactic and therapeutic interventions.

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Inflammatory neuropathies are a heterogeneous group of disorders of the peripheral nerves. Pathogenic antibodies targeting various antigens at the node-paranode junctions, leading to its disorganization, are increasingly recognized as accounting for an important subset of inflammatory neuropathies. Among these, antibodies against neurofascin (NF)155 and NF186 are the most widely recognized. The current study aimed to determine the prevalence of NF155 and NF186 antibodies in an Indian cohort of patients with inflammatory neuropathies. Seventy-six patients with inflammatory neuropathies, including 44 with Guillain-Barré syndrome (GBS) and 32 with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and 32 healthy controls were recruited. NF155 and NF186 antibodies were tested in sera from all study participants. In this study, 8/76 (10.53%) patients with inflammatory neuropathies tested positive for NF186 antibodies, including 5 (11.36%) with GBS and 3 (9.37%) with CIDP. Given the small sample size, definitive differences between the NF186 antibody-positive and antibody-negative groups could not be established. None of the patients with GBS and NF186 antibody positivity required mechanical ventilation. None of the patients with CIDP and NF186 antibody positivity had an acute GBS-like onset. One patient in the NF186 antibody-positive CIDP group had the phenotype of combined central and peripheral demyelination. None of the study participants tested positive for NF155 antibodies. A higher proportion of GBS patients showed NF186 reactivity in the present study than in previous reports. The spectrum of other pathogenic antibodies remains to be tested, as the majority of patients with inflammatory neuropathies tested negative for the two NF antibodies.

Toxoplasma gondii infects one-third of the global human population and invades and chronically persists in the central nervous system of the infected host. Chronic infection in the brain correlates with changes in the neuronal architecture and behavior. To the best of our knowledge, the association between T. gondii and neurological and psychiatric disorders has not been studied in the Indian population. Therefore, this study was conducted to determine the association between T. gondii in these patients. This cross-sectional study was conducted in a large Neuroscience Center by the Department of Microbiology in collaboration with the Psychiatry and Neurology Departments for 7 months from March to September 2025. A total of 281 neuropsychiatric patients and an equal number of controls were taken. They were further classified using the International Classification of Diseases, ICD-10 codes. After carefully explaining the procedure and goal of the study, informed written consent was taken. 3 mL of blood specimens was drawn under aseptic conditions by venipuncture, which was collected in sterile plain vials. Serum samples were tested for the presence of specific anti-T. gondii immunoglobulin G antibodies using a commercial qualitative enzyme-linked immunosorbent assay. Our results reveal a higher prevalence of T. gondii antibodies among schizophrenia (33.34%), mental and behavioral disorder due to substance abuse (30%), bipolar affective disorder (32%), Parkinson's disease (31.03%), and dementia (35%). Our results suggest that T. gondii seropositivity is higher among the psychiatric and neurological patients, but it is not significantly associated as compared to controls. Résumé Introduction:Toxoplasma gondii infecte un tiers de la population mondiale et envahit le système nerveux central de l’hôte infecté, où il persiste de façon chronique. L’infection chronique du cerveau est corrélée à des modifications de l’architecture neuronale et du comportement. À notre connaissance, l’association entre T. gondii et les troubles neurologiques et psychiatriques n’a pas été étudiée dans la population indienne. Par conséquent, cette étude a été menée afin de déterminer l’association entre T. gondii et ces troubles chez ces patients.Matériel et méthodes:Cette étude transversale a été menée dans un grand centre de neurosciences par le département de microbiologie, en collaboration avec les départements de psychiatrie et de neurologie, pendant 7 mois, de mars à septembre 2025. Au total, 281 patients neuropsychiatriques et un nombre égal de témoins ont été inclus. Ils ont ensuite été classés selon la Classification internationale des maladies (CIM-10). Après avoir expliqué en détail la procédure et l’objectif de l’étude, un consentement éclairé écrit a été obtenu. Un prélèvement sanguin de 3 mL a été effectué par ponction veineuse dans des conditions aseptiques, et recueilli dans des tubes stériles sans anticoagulant. Les échantillons de sérum ont été analysés pour la présence d’anticorps IgG anti-Toxoplasma gondii spécifiques à l’aide d’un test immuno-enzymatique (ELISA) qualitatif commercial.Résultats:Nos résultats révèlent une prévalence plus élevée d’anticorps anti-Toxoplasma gondii chez les patients atteints de schizophrénie (33,34 %), de troubles mentaux et comportementaux liés à la toxicomanie (30 %), de trouble bipolaire (32 %), de maladie de Parkinson (31,03 %) et de démence (35 %).Conclusion:Nos résultats suggèrent que la séropositivité à Toxoplasma gondii est plus élevée chez les patients psychiatriques etneurologiques, mais cette association n’est pas significative par rapport aux témoins.

Multisystem inflammatory syndrome in children (MIS-C) is associated with favorable short-term outcomes. However, long-term follow-up data are limited, particularly from low- and middle-income countries. This prospective follow-up study was conducted at a tertiary care hospital in North India between November 2024 and September 2025, involving children (n = 51) admitted with MIS-C and discharged between September 2020 and August 2022. The data collected included the clinical profile, echocardiography (left ventricular ejection fraction and coronary artery diameters), Screen for Child Anxiety-Related Disorders scale, UCLA Post-traumatic Stress Disorder Reaction Index and Vineland Social Maturity Scale. During the acute phase, common manifestations included fever, gastrointestinal and mucocutaneous involvement, shock, elevated inflammatory markers, myocardial dysfunction (47%) and coronary abnormalities (22%). At follow-up 44 (43-46) months after discharge, none had major clinical symptoms; all had normalized left ventricular ejection fraction, normal school performance and peer relationships; and only 12% had mild coronary artery abnormalities. There were no anxiety or post-traumatic stress disorder-related symptoms, and all had age-appropriate social maturity. Long-term outcomes of MIS-C are favorable, with complete recovery of myocardial function, persistent mild coronary abnormalities in a small proportion, no anxiety or post-traumatic stress disorder, and normal social maturation.

This article is a structured narrative review that synthesizes empirical findings and expert consensus and provides policy guidance to outline implementation pathways for integrating Yoga into mainstream healthcare systems, with India as a case example. Yoga is an ancient health practice traditionally used as a holistic approach to health management and wellbeing. However, the acceptance of Yoga as an evidence-based practice in the modern healthcare delivery requires systematic reassessment for its implementation within the healthcare system to make healthcare more affordable, improve prevention, rehabilitation, and resilience thus reduce strain on medical resources. In this review, we have organized the literature review and practical insights around three core themes: stakeholder configurations and governance, economic and quality management, and implementation strategies and evaluation to develop an actionable framework for an optimal care system responsive to patients' needs and adaptable to different community settings. This article has incorporated peer-reviewed studies on the effectiveness of Yoga, its implementation in mainstream healthcare, along with relevant publicly available policy, accreditation, and practice standard sources, to emphasize constructs of implementation science and evidence-based practice. The review identifies a know-do gap between growing evidence for Yoga and its system-level adoption, proposing a staged framework that integrates stakeholder engagement, economic evaluation, quality management, and monitoring to support evidence-based implementation. We propose a comprehensive, context-sensitive model that combines traditional wisdom with contemporary behavioral, clinical, and systems-based approaches. By embedding Yoga within an implementation science framework, we advocate for its role as a mainstream, evidence-informed system. Adoption of Yoga as a therapeutic and preventive modality can be accelerated through standardized protocols, transparent evaluation and regulation, and tripartite governance among state actors, healthcare institutions, and Yoga professionals; however, the feasibility hinges on context-sensitive financial support, stakeholder management, and workforce development.

Retinal artery occlusion (RAO) shares vascular pathophysiology with cerebrovascular disease, and its relationship to incident dementia remains unsettled. Reported associations may reflect shared vascular pathology, differential ascertainment along the intensive workup pathways that RAO patients enter, or both. No prior study has calibrated RAO-dementia estimates against prespecified negative-control outcomes spanning distinct ascertainment pathways. Among 129,279 All of Us participants aged 50 years or older and free of prevalent dementia (controlled-tier release R2024Q3R9, OMOP common data model), strict RAO was defined by seven verified SNOMED concept identifiers (n = 339). Incident dementia required two or more codes at least 30 days apart (Wilkinson algorithm), with prespecified vascular and Alzheimer subtypes. Cox models used age as timescale with left truncation and time-varying exposure; 1:5 propensity-score matching was the primary confounder-adjusted analysis. Cataract, benign paroxysmal positional vertigo (BPPV), and inguinal hernia were prespecified negative controls for ophthalmology, neurology, and general-contact pathways. There were 1,506 incident dementia events. RAO was not associated with all-cause dementia (unmatched hazard ratio (HR) 0.81, 95% confidence interval (CI) 0.40-1.64; matched HR 1.33, 95% CI 0.72-2.47; 10 exposed events). The vascular dementia estimate remained elevated but imprecise (unmatched HR 1.93, 95% CI 1.02-3.66; matched HR 1.81, 95% CI 0.66-4.94; 3 exposed events). Cataract was elevated (HR 1.87, 95% CI 1.45-2.42), whereas BPPV (HR 1.27, 95% CI 0.90-1.79) and hernia (HR 1.10, 95% CI 0.68-1.78) were not. We found no evidence that RAO is independently associated with incident dementia, replicating a large European null finding in a diverse United States cohort. The cohort was underpowered to exclude clinically meaningful effects, particularly for vascular dementia. Detection bias in this dataset was demonstrably pathway-specific, but same-pathway calibration accounts for only part of the residual vascular dementia estimate.

Dextromethorphan-associated neurotoxicity with cerebellar edema syndrome is a recently described clinico-radiological condition resembling pediatric opioid use-associated neurotoxicity with cerebellar edema syndrome. To describe two children with dextromethorphan-associated neurotoxicity with cerebellar edema syndrome from a tertiary care hospital in North India. The clinical details were obtained from the medical case records of the children admitted with dextromethorphan-associated neurotoxicity with cerebellar edema syndrome during the month of August and September 2025. We report two children (3 years and 13 months) who presented with encephalopathy following ingestion of dextromethorphan-containing cough syrup for viral prodrome. Magnetic resonance imaging showed T2/FLAIR hyperintensities in bilateral cerebellar hemispheres with diffusion restriction, suggestive of cytotoxic edema. With supportive treatment and intravenous methylprednisolone, both patients recovered rapidly with no residual neurologic deficits. These two cases highlight the occurrence of dextromethorphan-associated neurotoxicity with cerebellar edema syndrome in young children. Sensitization of healthcare providers about dextromethorphan-associated neurotoxicity with cerebellar edema syndrome, early clinical suspicion, confirmation of diagnosis with neuroimaging, and supportive care, may be associate with good neurological recovery. Dextromethorphan-associated neurotoxicity with cerebellar edema syndrome is a new clinico-radiological condition that occurs following ingestion of dextromethorphan in young children. Similar to the recently published report and cases presented here, early identification and treatment may be associated with favorable neurological recovery. Therefore, this syndrome should be considered in the differential diagnosis at an early stage. There is a need to increase awareness among healthcare providers to avoid prescribing dextromethorphan-containing cough syrups to younger children.

The relationship between statin therapy and clinical outcomes after intracerebral hemorrhage (ICH) remains uncertain. Therefore, we performed a post-hoc analysis of the third intensive care bundle with blood pressure reduction in acute cerebral haemorrhage trial study to evaluate the associations of pre-ICH and post-ICH statin use with clinical outcomes. The primary outcome was death or dependency (modified Rankin Scale [mRS] 3-6) at 6 months. Secondary outcomes included death, dependency, hematoma expansion, serious adverse events (SAEs), and cerebral hemorrhagic events. Adjusted odds ratios (aOR) with 95% confidence intervals (CI) were estimated. Analysis was performed using generalized linear mixed model. We further examined whether post-ICH statin therapy modified outcomes within the care bundle group. Overall, a total of 7035 patients were included in the study. Pre-ICH (aOR 0.93, 95% CI 0.61-1.42) or post-ICH statin use (aOR 0.97, 95% CI 0.72-1.29) was not associated with death or dependency. However, pre-ICH statin use was associated with lower 6-month mortality (aOR 0.46, 95% CI 0.26-0.80) and a reduced incidence of cerebral hemorrhage (aOR 0.45, 95% CI 0.21-0.97). In stratified analyses, post-ICH statin use was associated with lower odds of 6-month mortality or disability among care bundle recipients (aOR 0.66, 95% CI 0.44-0.99; P = 0.046), with significant effect modification by intervention allocation (P for interaction = 0.019). In summary, statin therapy before or after ICH onset appeared to be safe, without increased risk of SAEs and hematoma expansion. Besides, among patients receiving the care bundle intervention, post-ICH statin use showed a potential association with improved functional outcomes. These exploratory findings require confirmation in future studies.

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Neurological disorders (NDs) represent a significant and rapidly increasing global health problem, resulting in the progressive loss of neurons and cognitive decline. Current treatments are symptomatic and have major side effects. This review provides a detailed discussion on the roles and modes of action of the phytocompounds, their mechanistic pathways, and the challenges and opportunities, along with their clinical translation. Relevant literature published in peer-reviewed journals was collected from databases including PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar using keywords related to phytochemicals, neuroprotection, oxidative stress, inflammation, and neurological disorders. Studies focusing on the mechanistic and therapeutic roles of plant-derived bioactive compounds were critically analyzed. The application of different phytocompounds, including polyphenols, flavonoids, alkaloids, and terpenoids, is discussed. In addition, the roles and modes of action of phytocompounds such as curcumin, resveratrol, and epigallocatechin gallate (EGCG) have been discussed in relation to oxidative stress, inflammation, and protein aggregation. Their therapeutic actions are mediated via key mechanistic pathways, such as NF-κB inhibition, Nrf2/ARE activation, anti- apoptotic effects, neurotransmitter regulation, and chelation of redox-active metals. Emerging evidence suggests that phytochemicals may mitigate oxidative stress, neuroinflammation, and neuronal damage associated with NDs. However, variability in phytochemical composition and insufficient clinical validation remain major concerns. Phytochemicals possess multi-target neuroprotective activities and may serve as promising therapeutic candidates for NDs. Challenges and Future Directions: The existing limitations, such as poor bioavailability, lack of standardization, and regulatory barriers, prevent clinical translation. The recent advances, including nanocarrier-based delivery of plant-derived drugs, artificial intelligence-driven phytocompound modelling, and pharmacogenomics-based personalized therapy, have been discussed. Phytochemicals hold significant promise for neurotherapeutics. Nevertheless, their clinical application in several NDs requires advances in targeted drug delivery systems, precision medicine, standardized formulations, and robust mechanistic and clinical studies.

Spinocerebellar ataxia type 12 (SCA12) is a progressive late-onset neurodegenerative disorder caused by expansion of ≥ 43 trinucleotide CAG repeats in the upstream non-coding region of the PPP2R2B gene at locus 5q32 (SCA12; OMIM#604326). Clinically SCA12 patients predominately present hand tremor, gait ataxia, tremulous voice and other neurological and psychiatric features. Neuroimaging reveals degenerative changes in the cerebral cortex and cerebellum, however, the underlying disease mechanism at molecular level is still incompletely understood. Here we report generation of four induced pluripotent stem cells (iPSCs) of SCA12 patients. The established lines were positive for PPP2R2B-CAG expansion mutation and showed expression of undifferentiated hPSC state markers, three germ layer differentiation potential, normal genetic integrity and contamination-free culture.

KMT2A-rearranged (MLL-r) leukemias are highly aggressive hematological malignancies that require improved targeted therapies. DOT1L (histone H3K79 methyltransferase) functions as a critical oncogenic driver and represents an important therapeutic target in these high-risk leukemias. However, clinical responses to the first-in-class DOT1L inhibitor pinometostat (EPZ5676) have been modest, attributed to suboptimal pharmacokinetics and, more fundamentally, to the recognition that DOT1L possesses methyltransferase-independent functions that evade catalytic inhibition. This highlights the need for strategies that abrogate the full spectrum of DOT1L activity to effectively treat these high-risk leukemias. Proteolysis-targeting chimeras (PROTACs), which induce selective degradation of the DOT1L protein rather than inhibiting its catalytic activity, have therefore emerged as a promising approach. Notably, VHL-recruiting DOT1L PROTACs, such as DOT1L808, have demonstrated improved pharmacokinetic profiles and potent antileukemic activity in preclinical in vivo models. However, these findings remain preclinical, and significant challenges including oral bioavailability, potential toxicity, and lack of clinical validation must be addressed before clinical translation. In this review, we provide an overview of the evolving understanding of the biology of DOT1L, discuss existing MLL small molecule therapies, and evaluate current advances in therapeutically targeting DOT1L, with particular focus on the targeted degradation of DOT1L as a promising therapeutic strategy for high-risk KMT2A-r leukemia.

A cDNA sensor based on gold nanoparticles (Au) supported on nickel metal-organic framework nanosheets (MOF-NS) modified fluorine-tin oxide (FTO) glass electrode for the ultrasensitive and selective detection of miRNA-128 biomarker associated with the progression of Alzheimer's disease (AD) has been reported. The MOF-NS and Au nanoparticles were electrodeposited onto FTO electrode using chronoamperometry to immobilize 5'-biotinylated DNA (btn-cDNA) complementary to miRNA-128 by streptavidin-biotin interaction, generating the modified electrode (btn-cDNA/SV/Au/MOF-NS/FTO). The fabricated electrode was characterized using various surface characterization techniques, including FESEM, XPS, FTIR, and electrochemical methods. The fabricated electrode was then utilized for the selective detection of miRNA-128 using electrochemical impedance spectroscopy. The results indicated a linear response range of 1.0 × 10-1 fM-1.0 × 102 nM with limit of detection of 0.017 fM, and sensitivity of 180.11 Ω fM-1cm-2. Moreover, the cDNA sensor showed satisfactory performance with real serum samples from AD patients and healthy individuals, as validated by real time-PCR technique with area under curve of 0.93 and a sensitivity of 90%, respectively, demonstrating the potential of present cDNA sensing approach in the biomedical field.

Truenat MTB Plus assay along with dedicated chips for rifampicin and isoniazid can aid in TB elimination efforts by establishing diagnosis of drug-resistant extrapulmonary tuberculosis (EPTB). 600 EPTB samples (125 microbiologically-confirmed, 275 clinically-suspected and 200 controls) processed between January 2019 and June 2023 were subjected to Truenat MTB Plus for detection of Mycobacterium tuberculosis. All samples showing presence of M. tuberculosis were subjected to individual chips for rifampicin and isoniazid detection. They were also subjected to Xpert MTB/RIF Ultra assay (XpertUltra). The sensitivity, specificity, positive and negative predictive value of Truenat MTB Plus for detecting EPTB was 73.5%, 100%, 100% and 65.3%, respectively, while that of XpertUltra was 69.2%, 100%, 100% and 61.9%, respectively. Their performance was comparable (p = 0.087), though the overall agreement with composite reference standard was substantial for Truenat MTB Plus (κ = 0.64) and moderate for XpertUltra (κ = 0.60). 18 cases of EPTB were detected only by Truenat MTB Plus and one only by XpertUltra. TruRif reported all 18 cases of RifR while XpertUltra reported 14. Two cases of false-RifR and four of false-InhR were reported by drug chips of Truenat MTB Plus. Truenat MTB Plus, along with its chips for detecting drug resistance, outperformed XpertUltra as it not only detected 18 additional cases but also enabled detecting resistance to isoniazid, in addition to rifampicin.

Magnetic nanoparticles (MNPs) are becoming significant assets in cancer immunotherapy. Their unique magnetic and surface-functional properties allow them to serve as multifunctional platforms capable of modulating immune responses at multiple levels. MNPs have the potential to enhance immune cell activation and targeting inside the tumor microenvironment. MNPs assist in transporting immune-stimulating agents and tumor antigens directly to antigen-presenting cells. This increases T cell activity and improves anti-tumor reactions. MNPs are additionally utilized to enhance checkpoint blockade and to overcome the immunosuppressive milieu that often hinders the therapeutic efficacy of immunotherapies. In certain preclinical models, MNPs facilitate local hyperthermia to stimulate local immune activation at tumor sites. The magnetic guidance of these nanoparticles also facilitates the delivery of cytotoxic lymphocytes such as CD8 T cells and natural killer (NK) cells to solid tumors, addressing the challenge of poor infiltration of immune effector cells into the tumor. Numerous designs currently integrate therapy with imaging for accurate monitoring of biodistribution. Although MNPs hold potential, challenges remain in terms of biodegradability, long-term biosafety, immune compatibility and clinical applications. This review covers recent advances in MNP-based cancer immunotherapy, including their mechanisms of immune modulation, innovative design strategies, and integration with existing therapies. It also discusses the current limitations and future perspectives that will guide the next generation of magnetically assisted immunotherapeutic platforms toward clinical success.

Blood-brain barrier (BBB) dysfunction is an early feature of Alzheimer's disease (AD). Fibrinogen represents a sensitive marker of BBB leakage, but whether it modifies longitudinal tau progression in cognitively unimpaired (CU) individuals remains unknown. CU older adults underwent clinical evaluation and cerebrospinal fluid (CSF) assessment of fibrinogen, Aβ42, total tau (tTau), phosphorylated tau 181 (pTau181), and YKL-40. Linear regression tested baseline associations. Linear mixed-effects models tested whether baseline fibrinogen predicted longitudinal pTau181 change. Among 169 CU participants with baseline fibrinogen, 87 had longitudinal pTau181 measurements (mean follow-up 2.5-years). Higher fibrinogen was associated with elevated YKL-40 (β = 0.28, 95% confidence interval [CI] [0.11, 0.45]) but not Aβ42, tTau, or pTau181 at baseline. Baseline fibrinogen modified longitudinal pTau181 trajectories (interaction β = 0.11, 95% CI [0.04, 0.19]), with only participants above the median showing significant pTau181 increases (β = 0.13, 95% CI [0.08, 0.18]). CSF fibrinogen associates cross-sectionally with glial inflammation and predicts accelerated tau accumulation in preclinical AD.

We present a rare case of striatal encephalitis associated with small cell lung cancer (SCLC), manifesting as a choreiform movement disorder. A 57-year-old woman presented with a subacute onset of involuntary movements. Despite extensive investigations, the etiology of this choreiform movement disorder remained elusive until a detailed evaluation of clinical signs and radiological findings revealed SCLC. In addition, she had an asymptomatic metastatic brain parenchymal lesion. This case highlights the importance of considering paraneoplastic striatal encephalitis (PSE), a rare presenting neurological syndrome.