NeuroSci

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/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.