Research has documented a high prevalence of cognitive and affective impairments in individuals with spinal cord injury (SCI). However, the molecular mechanisms underlying these deficits remain poorly understood. In this study, to investigate the molecular basis of cognitive and affective dysfunctions following SCI, we examined the role of calcium/calmodulin-dependent kinase II (CaMKII) activation, with a specific focus on its phosphorylated form (pCaMKII), using a rat model of SCI.
Experimental results demonstrated that SCI led to spatial memory deficits as well as depression- and anxiety-like behaviors, as evidenced by performance in the Morris water maze (MWM), elevated plus maze (EPM), and forced swim test (FST). Compared to the sham group, increased levels of pCaMKII were observed in the medial prefrontal cortex (mPFC) at Day 56 after SCI. Moreover, inhibiting CaMKII phosphorylation via microinjection of KN-93—a CaMKII activation inhibitor—into the mPFC alleviated depression-like behavior and cognitive deficits, but not anxiety-like behavior.
These findings suggest that CaMKII activation in the mPFC may play an important role in mediating negative emotional states following SCI.
Poststroke cognitive impairment (PSCI) is a common functional disorder that occurs following stroke, but there are few effective therapies. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive neuromodulatory technique that has been used to improve cognitive function in stroke patients. Despite its widespread use in clinical research, the underlying mechanisms of rTMS are largely unknown. This study hypothesized that rTMS ameliorates PSCI by regulating white matter injury, which is of vital importance in cerebral ischemia.
An ischemic stroke rat model was created using transient middle cerebral artery occlusion. The extents of brain damage and white matter injury, including diffusion tensor imaging and diffusion tensor tractography, were evaluated using MRI. Behavioral tests, including the modified neurological severity score test and Morris water maze test, were also used. In addition, we preliminarily explored the potential role of SDF-1α/CXCR4 by Western blot analysis and real-time reverse transcription PCR.
The results showed that 10 Hz rTMS promoted neurological recovery and cognitive deficits in ischemic rats. Additionally, 10 Hz rTMS alleviated cerebral infarct severity and attenuated white matter lesions. Furthermore, the expression levels of components of the SDF-1α/CXCR4 axis influenced the effect of rTMS on ischemic stroke.
This research provides further evidence that 10 Hz rTMS can alleviate white matter injury in affected brain regions and improve PSCI after ischemic stroke, potentially through the activation of the SDF-1α/CXCR4 axis.
Migraine is a prevalent neurological disorder causing significant suffering and imposing a substantial burden on healthcare systems. Utilizing data from the Global Burden of Disease Study (GBD) 2021, this study comprehensively analyzes the current status, historical trends (1990–2021), and future projections of migraine burden in China and other G20 countries. The aim is to provide scientific evidence to inform evidence-based health strategies.
We analyzed GBD 2021 data to calculate migraine incidence, prevalence, disability-adjusted life years (DALYs), and years lived with disability (YLDs) from 1990 to 2021. Statistical analyses characterized these metrics across age, sex, year, geographical region, and the sociodemographic index (SDI). Trends in China and other G20 countries were tracked. Future trends (2022–2050) were projected using exponential smoothing (ES) and autoregressive integrated moving average (ARIMA) models. The Bayesian age-period-cohort (BAPC) model quantified the effects of age, period, and cohort factors on incidence, elucidating long-term burden drivers.
Migraine burden exhibited significant age dependency, with a bimodal age pattern. A pronounced gender disparity was evident, with females bearing a consistently higher burden across all metrics (e.g., prevalence approximately twice that of males). From 1990 to 2021, the migraine burden demonstrated a dual-track trajectory: An overall increase in total burden accompanied by a widening gender gap. Predictive models project a concerning future: Without effective interventions, the migraine burden during 2030–2050 will feature further escalation of the gender imbalance. The BAPC model indicates a projected century-long intensification of the migraine burden.
The migraine disease burden possesses distinct age and sex dimensions, revealing significant disparities across SDI regions, countries, age groups, and genders. The escalating burden necessitates targeted interventions and public health initiatives, particularly in regions and populations disproportionately affected.
Alzheimer's disease (AD), the leading cause of dementia, is characterized by amyloid-β accumulation, tau hyperphosphorylation, neuroinflammation, and synaptic failure, with no curative therapies available. This review aims to explore innovative therapeutic and diagnostic strategies, focusing on mesenchymal stem cell–derived exosomes (MSC-exos) as potential disease-modifying agents.
The review synthesizes current evidence on the regenerative, immunomodulatory, and neuroprotective properties of mesenchymal stem cells (MSCs) and their exosomes. It examines how MSC-exos, as nanosized extracellular vesicles carrying proteins, lipids, and nucleic acids, interact with the central nervous system to modulate disease pathways.
MSC-exos can cross the blood–brain barrier (BBB), deliver neurotrophic factors, modulate microglial activity, enhance amyloid clearance, and support neuronal survival and synaptic plasticity. They also hold promise as biomarkers by reflecting central nervous system pathology in peripheral biofluids. Early clinical trials using MSCs from bone marrow, adipose tissue, and umbilical cord show safety and feasibility, with exosome-based approaches offering scalable, cell-free alternatives.
MSC-derived exosomes present a promising avenue for both therapeutic intervention and early diagnosis in AD, offering neuroprotective, anti-inflammatory, and pro-regenerative effects. However, further progress requires addressing challenges such as exosome isolation standardization, cargo characterization, and regulatory considerations to enable their translation into clinical practice.
St. John's wort (Hypericum perforatum) has been used for centuries as a medicinal plant to remedy external disorders such as burns and wounds, as well as internal disorders such as nerve pain, anxiety, and depression. Bone marrow mesenchymal stem cells (BMSCs) are a heterogeneous population of pluripotent stromal cells that can differentiate into a variety of cell types. The aim of the study was to individually and combinationally investigate the effect of whole extract and stem cells on Parkinson's disease. Furthermore, using a new method for stem cells transplantation to enhance cell integration into substantia nigra pars compacta (SNC) and striatum.
In the study, 63 adult male Wistar rats were classified, and among them, treatment groups received 20 mg/kg extract (intraperitoneally; 28 days) and nearly 1 million (mean of 936 × 103) mesenchymal stem cells through cisterna magna, either individually or in combination.
Histological evaluations revealed that there has been a sharp rise in neurons in both ventral and dorsal striatum in the pretreatment plus cell group (p < 0.001). Regarding neurons in SNC area, quantitative investigations via Nissl and immunohistochemistry staining showed significant differences between the lesion group and groups receiving pretreatment, treatment plus cells, and pretreatment plus cells (p < 0.001). According to evidence, there are some communications between St. John's wort and stem cells that have led to navigate stem cells to immigrate and deploy within striatum.
The study found that both H. perforatum extract and BMSCs can help preserve dopaminergic neurons and glial cells during which combination therapy demonstrates synergy as an indicator. St. John's is a natural preserver and appears to function as a neuroprotective agent and facilitate the navigation and integration of stem cells; consequently, it keeps surviving both neurons and glial cells against pathogens and destructive environmental factors and has a potential to help us and Parkinson's patients.
To critically synthesize the current understanding of narcolepsy's pathophysiology, diagnostic challenges, and treatment landscape, and to articulate the emerging paradigm shift from symptomatic management toward disease modification.
This narrative review is based on a strategic search of literature from PubMed and Google Scholar published between 2015 and 2025, focusing on disease mechanisms, diagnosis, and established and emerging therapeutic interventions.
Narcolepsy is a neurological disorder fundamentally driven by an irreversible loss of hypocretin-producing neurons, a process strongly linked to an autoimmune response in individuals with the HLA-DQB1*0602 allele. Despite this well-defined pathophysiology, diagnosis is often delayed by nearly a decade due to limited physician awareness and symptom overlap with a wide range of psychiatric and metabolic comorbidities. Current pharmacological strategies, while providing partial relief from excessive daytime sleepiness and cataplexy, are purely symptomatic and fail to address the core hypocretin deficiency. The field is now at a critical inflection point, with promising research into hypocretin receptor agonists, targeted immunotherapies, and neuromodulation techniques poised to directly address the underlying pathology.
The existing therapeutic approach to narcolepsy is palliative, not restorative, leaving a significant unmet need for interventions that can alter the disease's natural history. The future of narcolepsy management depends on translating novel pathophysiological insights into disease-modifying therapies. Achieving this requires a concerted effort to accelerate diagnosis, validate new clinical endpoints, and prioritize the development of interventions capable of restoring neurological function. Such an approach holds the potential to move beyond symptom suppression and fundamentally improve the lives of individuals with narcolepsy.
There is a complex and interacting relationship between visual acuity, cognitive dysfunction, and frailty. It is suggested that frailty may mediate the relationship between visual acuity and cognitive impairment in older adults.
This study aimed to examine the mediating role of frailty in the relationship between visual acuity and cognitive function in older adults with visual impairment.
This cross-sectional correlational study was conducted with 116 participants with visual impairment at an ophthalmology clinic in Turkey between January and February 2025. Data were collected using an information form, the Standardized Mini-Mental Test, and the Edmonton Frailty Scale. Visual acuity was expressed as a logMAR score, ranging from 1.00 to −0.30.
The mean age of the participants was 70.92 ± 5.92. The logMAR score positively and significantly associated with frailty levels (p < 0.001). Frailty was found to have a significant negative effect on cognitive function (p < 0.001). In addition, a significant negative relationship was identified between cognitive function and the logMAR score (p < 0.01). Both the total and direct effects of the logMAR score on cognitive function were significant (p < 0.001). The indirect effect, tested using the bootstrap method, was also significant (Coeff = −5.304, BootSE = 1.079, 95% CI [−7.652, −3.462]).
These results suggest that the deterioration of visual acuity strongly impacts cognitive function and that frailty may mediate this relationship. Protecting visual health and preventing frailty in older adults may play a critical role in reducing the risk of cognitive impairment. Regular eye examinations, early intervention for vision disorders, and frailty prevention strategies can contribute to maintaining cognitive health.
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