NeuroSci最新文献

Background/aim: Vitamin D (VitD) has been implicated in neuroprotection, yet its role in Parkinson's disease (PD) remains unclear. This systematic review and meta-analysis aimed to evaluate the association between VitD status, supplementation, and vitamin D receptor (VDR) gene polymorphisms with PD risk and outcomes.

Methodology: Following PRISMA guidelines, we searched PubMed, Scopus, and Google Scholar through August 2025 for observational studies, clinical trials, and genetic association studies. Primary outcomes included serum VitD levels in PD versus healthy controls (HCs), prevalence of VitD insufficiency/deficiency, and effects of VitD supplementation on motor symptoms. Secondary outcomes assessed associations between VDR polymorphisms and PD susceptibility. Data were synthesized using random- and fixed-effects models, with heterogeneity and publication bias evaluated. PROSPERO (CRD420251133875).

Results: Sixty-three studies (n ≈ 10,700 participants) met inclusion criteria. PD patients exhibited significantly lower VitD levels (SMD = -0.46; 95% CI: -0.51 to -0.41) and higher odds of insufficiency (OR = 1.52) and deficiency (OR = 2.20) compared to HC. Cohort data suggested sufficient VitD may reduce PD risk (HR = 0.83). Supplementation yielded modest, non-significant improvements in motor outcomes. Among 20 genetic studies, FokI (rs2228570) was most consistently associated with PD, while other VDR SNPs showed variable or null associations.

Conclusions: VitD deficiency is common in PD and may influence disease risk and motor function. Current evidence indicates limited benefit of supplementation for motor outcomes, and genetic associations remain inconsistent.

Background: Cardiovascular diseases (CVD) affect the heart and blood vessels. Cardiorenal syndrome (CRS) highlights the interaction between the heart and kidneys, worsening the clinical course. Assessing renal function is essential for risk stratification and guiding therapeutic decisions. Furthermore, cognitive and psychological aspects are often impaired in these patients.

Aim: To compare clinical, cognitive, emotional, and quality of life parameters between patients with CRS and those with heart failure (HF) alone, and to assess the agreement between estimated glomerular filtration rate equations (Cockcroft-Gault and CKD-EPI).

Methods: This observational study was conducted at the Cardiology Unit of the IRCCS Centro Neurolesi Bonino Pulejo "Piemonte" Hospital (Messina, Italy) between June 2024 and March 2025. Thirty participants aged 45-85 years were enrolled: 15 with type 1 cardiorenal syndrome (CRS group) and 15 with heart failure without cardiorenal syndrome (HF group). All participants had a confirmed diagnosis and provided informed consent. Clinical evaluation and standardized tests (MoCA, BDI-II, BAI, and SF-12v2) were administered. Statistical analyses were performed using t-tests, chi-square tests, and Bland-Altman analysis, with significance set at p < 0.05.

Results: The two groups were comparable in body mass index and left ventricular ejection fraction. CRS patients had significantly higher serum creatinine and lower GFR with both equations. The two GFR equations were strongly correlated (r = 0.94; p < 0.0001). Bland-Altman analysis showed a mean difference of 5.80 mL/min (95% limits of agreement: -12.4 to +24.0 mL/min), indicating wide individual variability. No significant differences were found in cognitive performance or quality of life. However, CRS patients exhibited significantly higher depressive symptoms (BDI-II mean 11.33 ± 8.19 vs. 5.40 ± 6.68; p = 0.0384) and a trend toward higher anxiety (BAI mean 8.13 ± 4.73 vs. 4.67 ± 5.79; p = 0.0834).

Conclusions: A multidisciplinary approach, including psychological support, is necessary for patients with CRS.

The journal retracts the article "Cytotoxic Effect of Amyloid-β1-42 Oligomers on Endoplasmic Reticulum and Golgi Apparatus Arrangement in SH-SY5Y Neuroblastoma Cells" [...].

This study evaluated participation outcomes one year after aneurysmal subarachnoid hemorrhage (aSAH) compared with matched healthy controls and identified factors associated with participation within the patient group. Forty aSAH survivors and seventy-five controls were assessed 12-14 months post-ictus. Participation was measured with the Utrecht Scale for Evaluation of Rehabilitation-Participation (USER-P), psychological distress with the Hospital Anxiety and Depression Scale (HADS), coping with the Brief COPE, and cognition with the Montreal Cognitive Assessment (MoCA). Compared with controls, patients reported greater participation restrictions (82 vs. 100, p < 0.001), lower frequency (35 vs. 51, p < 0.001), and reduced satisfaction (65 vs. 75, p < 0.001). Anxiety, depression, and avoidant coping independently predicted restrictions (adjusted R² = 0.48), while satisfaction was predicted by employment, fewer depressive symptoms, and less avoidant coping (adjusted R² = 0.52). Lower MoCA scores predicted reduced participation frequency (p = 0.032), and patients with cognitive impairment showed significantly greater restrictions and lower satisfaction. One year after aSAH, survivors experience substantial participation limitations associated with psychological distress, maladaptive coping, and cognitive deficits. These results underscore the importance of cognitive and psychological rehabilitation to enhance long-term participation and social reintegration after aSAH.

Ever since the discovery that neuronal tissue can utilize lactate as an aerobic substrate for mitochondrial adenosine triphosphate (ATP) production, a debate has ensued between those who have questioned the importance of lactate in brain energy metabolism and those who argue that lactate plays a central role in this process. The "neuron astrocyte lactate shuttle hypothesis" has sharpened this debate since it postulates lactate to be the oxidative energy substrate for activated neurons. Those who minimize lactate's role insist that a non-oxidative process they termed "aerobic glycolysis" supports brain activation, despite oxygen availability. To explain the paradox that the active brain would utilize the inefficient glycolysis over the much more efficient mitochondrial oxidative phosphorylation (OXPHOS) for ATP production, they suggested the "efficiency tradeoff hypothesis," where the inefficiency of the glycolytic pathway is traded for speed necessary for the information transfer of the active brain. In contrast, other studies reveal that oxidative energy metabolism is the process that supports brain activation, refuting both the "aerobic glycolysis" concept and the premise of the "efficiency tradeoff hypothesis". These studies also shed doubts on the usefulness of the blood oxygenation dependent functional magnetic resonance imaging (BOLD fMRI) method and its signal as an appropriate tool for the estimation of brain oxygen consumption, as it is unable to detect any oxygen present in the extravascular brain tissue.

Per- and polyfluoroalkyl substances are persistent environmental contaminants increasingly implicated in neurotoxicity. Establishing causality and mechanisms relevant to Alzheimer's disease, Parkinson's disease, and multiple sclerosis requires human-relevant systems that capture exposure, barrier function, and brain circuitry. We review advanced cellular platforms-iPSC-derived neuronal and glial cultures, cerebral and midbrain organoids, and chip-based microphysiological systems-that model disease-relevant phenotypes (Aβ/tau pathology, dopaminergic vulnerability, myelination defects) under controlled PFAS exposures and defined genetic risk backgrounds. Modular, fluidically coupled BBB-on-chip → brain-organoid microphysiological systems have been reported, enabling chronic, low-dose PFAS perfusion under physiological shear, real-time barrier integrity readouts such as transepithelial/transendothelial electrical resistance (TEER), quantification of PFAS partitioning and translocation, and downstream neuronal-glial responses assessed by electrophysiology and multi-omics. Across platforms, convergent PFAS-responsive processes emerge-mitochondrial dysfunction and oxidative stress, lipid/ceramide dysregulation, neuroinflammatory signaling, and synaptic/network impairments-providing a mechanistic scaffold for biomarker discovery and gene-environment interrogation with isogenic lines. We outline principles for exposure design (environmentally relevant ranges, longitudinal paradigms), multimodal endpoints (omics, electrophysiology, imaging), and cross-lab standardization to improve comparability. Together, these models advance the quantitative evaluation of PFAS neurotoxicity and support translation into risk assessment and therapeutic strategies.

Mild traumatic brain injury (mTBI) frequently causes subtle brain changes that are difficult to detect with conventional diagnostic approaches. In this exploratory pilot study, we combined tri-exponential intravoxel incoherent motion (IVIM) and pseudocontinuous arterial spin labeling (pCASL) MRI with Multimodal Canonical Correlation Analysis and joint independent component analysis (mCCA+jICA) to identify imaging signatures distinguishing mTBI patients from healthy controls (HCs) and their associations with clinical function. Cerebral blood flow (CBF) and IVIM-derived metrics were extracted from 90 brain regions in 19 mTBI patients and 24 HCs, and multivariate components were identified using mCCA+jICA. Two independent components (IC2, IC15) showed group differences at the uncorrected level (p < 0.05) but did not survive false discovery rate (FDR) correction. IC2 correlated positively with CBF and perfusion fraction (F_p) and negatively with tissue diffusion fraction (F_s), consistent with reduced vascular integrity in mTBI, while IC15 showed similar trends. One component correlated with Glasgow Outcome Scale-Extended (GOS-E) scores (uncorrected p = 0.046). Although this study is preliminary and limited by a small sample size, our findings suggest that mTBI is associated with perfusion and microstructural alterations, particularly in subcortical regions, and demonstrate the potential value of combining IVIM and ASL within multivariate fusion frameworks to reveal patterns not captured by single-modality approaches.

Background: Glioblastomas (GBMs) in eloquent areas, particularly within the motor system, represent a significant surgical challenge due to the risk of postoperative neurological deficits. This study evaluates the effectiveness of a structured preoperative protocol, including nTMS-guided motor mapping, to optimize surgical outcomes and minimize neurological deficits, with a particular focus on the timing of adjuvant oncological therapy initiation.

Methods: A retrospective analysis was conducted on 44 GBM patients, divided into two groups: 11 with motor area lesions (group A) and 33 with non-eloquent lesions (group B). All patients underwent a standardized preoperative protocol. Surgical outcomes (EORs), neurological function (MRC score and KPS index), time to oncological therapy initiation and survival (OS and PFS) were compared between groups.

Results: Both groups achieved high rates of GTR without significant differences in EOR (72.7% group A vs. 78.8% group B). Although group A exhibited a higher incidence of postoperative motor deficits, motor function at three-month follow-up was similar between groups. Time to initiation of oncological therapy did not differ between groups (40.6 days group A vs. 41.9 days group B, p = 0.719), highlighting that preservation of motor function helped minimize delays in starting oncological therapy. No significant differences were found in survival outcomes.

Conclusions: A structured preoperative protocol incorporating nTMS motor mapping allows for safe and aggressive resection of motor-area GBMs. This approach effectively mitigates the risk of delays in initiating adjuvant oncological therapy, optimizing the patient prognosis. Further studies are needed to explore the long-term benefits of this protocol in both functional and oncological outcomes.

Several recent studies have utilized neuroimaging to delineate the localization and function of brain regions involved in language. However, many uncertainties persist regarding the organization of the linguistic system in the human brain. The aim of the present study was to characterize the structural changes produced in a sample of 9 patients with post-stroke aphasia (4 women; mean age = 60 years, SD = 14.86) and their relationship with performance in the entire Boston Diagnostic Aphasia Examination (BDAE). Magnetic Resonance Imaging was acquired from the brain of each patient and brain lesions were assessed. Disconnection's severity of each white matter tract by embedding the lesion into the streamline tractography atlas of the Human Connectome Project was analyzed, and grey matter lesion load using a 7-Network Cortical parcellation template was estimated, with additional subcortical, cerebellar and brainstem parcels. Finally, all data obtained was correlated with performance in the BDAE. Somatomotor network correlated with repetition scale. The disconnection of the left acoustic radiation and inferior longitudinal fasciculus correlated with repetition sub-scale. Finally, the left U-fibers correlated with severity (a BDAE sub-scale that assesses the patient's communicative skills), conversational speech and reading sub-scales. These findings emphasized that the disconnection of these fronto-parieto-temporal structures correlate with deficits in repetition, beyond the classical hypothesis attributing such deficits solely to the impairment of the arcuate fasciculus.

Stroke is the second-largest cause of death and disability worldwide, and many patients require intensive care for airway compromise, hemodynamic instability, cerebral edema, or systemic complications. This review summarizes key aspects of ICU management in both acute ischemic stroke (AIS) and hemorrhagic stroke (HS). Priorities are airway protection, oxygenation, individualized blood pressure targets, and strict control of temperature and glucose. Neurological monitoring and prompt management of intracranial pressure (ICP), together with timely surgical interventions (hemicraniectomy or hematoma evacuation), are central to acute care. Seizures are treated promptly, while routine prophylaxis is not recommended. Prevention of aspiration pneumonia, venous thromboembolism, infections, and other intensive care unit (ICU) complications is essential, along with early nutrition, mobilization, and rehabilitation. Prognosis and decisions about intensity of care require shared discussions with families and involvement of palliative services, when appropriate. Many practices remain based on observational data or extrapolation from other populations, underlining the need for stroke-specific clinical trials. Outcomes are consistently better when patients are managed in specialized stroke or neurocritical care units with a multidisciplinary treatment approach.