NeuroSci最新文献

Neurodegenerative diseases such as Alzheimer's, Parkinson's, amyotrophic lateral sclerosis, and Huntington's disease represent a major challenge in neuroscience due to their complex, multifactorial nature and the absence of curative treatments. These disorders share common molecular mechanisms, including oxidative stress, mitochondrial dysfunction, proteostasis collapse, calcium dyshomeostasis, chronic neuroinflammation, and the prion-like propagation of misfolded proteins. Together, these processes trigger a cascade of cellular damage that culminates in synaptic dysfunction and programmed neuronal death. This review integrates current evidence on the sequential stages of neurodegeneration, emphasizing the convergence of oxidative, inflammatory, and proteotoxic pathways that drive neuronal vulnerability. Moreover, it explores emerging therapeutic strategies aimed at restoring cellular homeostasis, such as Nrf2 activation, modulation of the unfolded protein response (UPR), enhancement of autophagy, immunotherapy against pathological proteins, and gene therapy approaches. The dynamic interplay among mitochondria, endoplasmic reticulum, and glial cells is highlighted as a central element in disease progression. Understanding these interconnected mechanisms provides a foundation for developing multi-targeted interventions capable of halting or delaying neuronal loss and improving clinical outcomes in neurodegenerative disorders. This work provides an integrative and introductory overview of the convergent mechanisms underlying neurodegeneration rather than an exhaustive mechanistic analysis.

In non-vasculitic immune-mediated neuropathies, imaging studies demonstrate an enlargement not only of clinically involved but also of clinically intact nerves. The present study aimed to present a pattern of nerve swelling and its relation to nerve function. In a group of patients with dysimmune motor and sensorimotor mononeuropathies, nerve cross-sectional areas (CSAs) were measured using ultrasonography (US) and compound muscle action potential (CMAP) amplitudes using electrodiagnostic (EDx) studies. Nerve CSAs were compared in (1) clinically involved, (2) swollen and clinically uninvolved, and (3) non-swollen (clinically uninvolved) nerves. Patients' non-swollen nerves were also compared to those of controls. In swollen nerves, the correlation between nerve CSA and CMAP amplitude was calculated. Twenty-two patients (12 men) and 50 controls (28 men) were included in the study. Clinically involved nerves were thicker than swollen segments of clinically intact nerves (p < 0.001). The patients' non-swollen (clinically uninvolved) nerves were thicker than the controls'. In swollen nerves, CSA was strongly negatively correlated with CMAP amplitude (r = -0.54, p < 0.001). In patients with immune-mediated mononeuropathies, nerve swelling correlates with clinical and EDx findings. Patients' clinically uninvolved nerves were also swollen, but to a lesser degree.

REM sleep behavioral disorder (RBD) is of increasing interest in Parkinson's disease (PD). Previous studies exploring the association between REM sleep without atonia (RWA) and clinical PD features or other objective sleep metrics are scarce and have used PSG findings. A mobile electroencephalography (EEG)/electrooculography (EOG) recording system with two channels can objectively measure sleep parameters, including RWA, during natural sleep at home. We investigated whether RWA measured on a portable recording device at home could be associated with clinical PD features or other sleep metrics using baseline data from the ZEAL study. Differences between patients with and without RWA was analyzed using ANCOVA test. REM sleep length was significantly longer in patients with RWA than in those without RWA. A multivariate comparison using ANCOVA showed a significant difference in log-transformed REM sleep duration of patients with RWA after adjustment for potential confounders (adjusted mean difference of 1.203; 95% confidence interval 0.468 to 1.937; p = 0.003). The strength of this study was that it evaluated the association between RWA during natural sleep at home and clinical variables as well as other sleep metrics. The major result was that patients with and without RWA did not differ in their clinical variables, and there was no relation between RWA and objective sleep metrics other than REM sleep. The duration of REM sleep may be associated with RWA during natural sleep at home.

Religious experiences represent a universal and timeless phenomenon that has accompanied humanity since its origins. In recent decades, neuroscience has explored the relationship between temporal lobe epilepsy (TLE) and hyperreligiosity phenomena, describing sudden convictions, states of ecstasy, and spiritual conversions associated with epileptic seizures. This article offers a narrative review of the literature on the relationship between epilepsy and religion, including its clinical manifestations (ictal, postictal, and interictal) and the main neurobiological models proposed to explain it, such as the limbic marker hypothesis and theory of mind (ToM). The possible role of the uncinate fasciculus as an integrative pathway between temporal and limbic regions is also explored, based on recent neuroimaging studies. Finally, we present an illustrative clinical case of a patient with meningioma and TLE associated with episodes of intense religious conviction, in whom a structural alteration of the right uncinate fasciculus was observed. This case reinforces the relevance of considering both neuronal networks and white matter tracts in the study of religious experiences, while underscoring the need for broader and more systematic studies to confirm these findings.

The experience of childhood maltreatment (CM) increases the risk for depressive disorders by two-and-a-half times across the lifespan. Although stress system and immunological models offer some explanation of this vulnerability, further investigation is required to understand the underlying neurophysiological mechanisms and identify potential biomarkers for diagnosis and treatment. Resting-state electroencephalography (EEG) offers a low-cost, non-invasive, and accessible methodology for that purpose. This narrative review synthesizes resting-state EEG findings that are common to CM and depression as a primer for further research and the future formulation of a model that may link these two in a causal manner. Although evidence supports atypical beta and theta band power, frontal alpha asymmetry and altered default mode network functional connectivity as possible indicators of the CM-EEG association, there is a paucity of EEG-based CM research available to complement the extensive depression-focused literature. Large-sample, prospective EEG studies of CM that consider confounding factors and assess the neurophysiological impact of CM independent of psychopathologies are required.

Mild cognitive impairment (MCI) is a nosological entity that requires special attention from a therapeutic perspective, because annual conversion rates to dementia of 5-15% in these cases are considered typical. This narrative review aimed to identify available data supporting the efficacy and tolerability of various pharmacological therapeutic interventions by searching PubMed/MEDLINE, the Cochrane Database of Systematic Reviews, and the Web of Science (WoS) Core Collection for primary and secondary reports published over the last 25 years on the pharmacological treatment of MCI. The retrieved interventions were distributed in five large categories: (1) conventional cognitive enhancers; (2) disease-modifying therapeutic interventions; (3) strategies mitigating vascular risk and management of concomitant medications; (4) adjuvant and nootropic formulations; (5) case management of non-cognitive symptoms in MCI. The most broadly applicable pharmacological strategies in MCI include systematic deprescribing and optimisation of concomitant therapies, reducing anticholinergic and sedative load, avoiding iatrogenic hypoglycaemia and excessive blood pressure lowering, and careful, individualised treatment of vascular risk factors. Based on the randomised controlled trials, meta-analyses, and contemporary guidelines, a pragmatic pharmacological approach to MCI is suggested. Further trials with better design are urgently needed to document the efficacy and safety of pharmacological interventions in patients diagnosed with MCI.

Objectives: The aim of this study was to investigate the effectiveness of Cryoflow cooling on forearm skin temperature and nerve conduction velocity (NCV) in normal subjects. Methods: Thirty male volunteers participated in this study, with a mean age of 20.8 ± 0.74 years. A Cryoflow hose with a nozzle was positioned approximately 10 cm from the forearm and scanned the anterior surface of the non-dominant forearm for 10 min, with temperatures adjusted to -10 °C. Participants' average skin temperature was measured by using an infrared camera. Motor and sensory NCV for both the median and ulnar nerves were measured from both forearms. The dominant side served as a control side. The level of significance was set at p value ≤ 0.05. Results: Following treatment, the experimental group experienced a reduction in average skin temperature, dropping from 32.94 ± 1.11 °C to 16.92 ± 1.68 °C, while the control group showed no significant change. Both the median and ulnar nerves exhibited significant decreases in motor NCV (-10.37 m/s and -8.79 m/s, respectively), alongside slight increases in distal motor latency. Sensory NCV of the median and ulnar nerves decreased significantly (-5.20 m/s and -8.40 m/s, respectively), accompanied by increased onset latency. No significant changes were found in the control group. Conclusions: Cryoflow air-based cryotherapy to the forearm causes a substantial reduction in local skin temperature and significant slowing of peripheral nerve conduction. Both motor and sensory fibers of the median and ulnar nerves exhibited decreased conduction velocities and increased latencies following cooling.

Background: Innovative treatments for lung cancer patients have significantly improved their lives. Therefore, patients who develop brain metastases are more likely to require management of quality of life (QoL) by reducing pathological decline in brain function. New therapeutic strategies have allowed us to manage brain metastases, thanks to the ability to cross the blood-brain barrier. Moreover, new molecules have been designed as adjuvants to standard treatments for the management of cancer patients with brain metastases.

Methods: We implemented a descriptive, observational, retrospective study. Therefore, we consecutively collected the data of eighty-six (N  =  86) patients admitted to our department (April 2020-April 2025) diagnosed with brain involvement in a thoracic neoplasm and treated with silibinin, in association with standard treatment. The main endpoint of our analysis is to define the safety profile of silibinin and to evaluate its eventual benefits in terms of QoL.

Results: Silibinin was well tolerated (only one mild adverse event was reported); furthermore, patients taking silibinin had a good quality of life that was maintained over a long period of time, and in some cases, an improvement in neurological symptoms and overall patient well-being was also documented.

Conclusions: Our study is the first collection of a large number of lung cancer patients with brain metastasis taking silibinin, which is very well tolerated and allows patients to maintain a good QoL.

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.