Neurological Research最新文献

Background: Carotid artery stenosis (CAS) reduces cerebral blood flow and is frequently associated with cognitive impairment and reduced quality of life (QoL), particularly in severe CAS. Although carotid revascularization (stenting or endarterectomy) can improve blood flow and potentially enhance cognitive function and QoL, the impact of CAS before revascularization remains unclear.

Objective: This review aimed to synthesize the literature exploring the relationship between CAS, cognitive impairment, and QoL, focusing on pre-revascularization outcomes.

Method: A comprehensive scoping review was conducted using PubMed, CINAHL, MEDLINE, EMBASE, PsycINFO, EBSCO, and Scopus to identify relevant studies published between 2015 and 2023.

Results: This review identified consistent evidence linking severe CAS (≥70%) to significant cognitive decline, particularly in areas such as memory, attention, and executive function. Although carotid revascularization showed promise in improving cognitive performance, the extent of recovery varied. Studies also highlighted the profound impact of CAS on QoL, with patients frequently experiencing anxiety, depression, and physical limitations. While revascularization procedures were associated with improvements in physical functioning and overall well-being, emotional recovery often delayed.

Conclusion: CAS substantially affects both cognitive functioning and QoL, even before revascularization. Although some studies suggested that revascularization may lead to improvements in cerebral perfusion and certain domains of cognitive function, the trajectory of psychosocial and emotional recovery; including depressive symptoms, anxiety, and fear of future cerebrovascular events, demonstrates delayed improvement. These emotional outcomes mediate overall QoL and should be a focus of both clinical assessment and future longitudinal studies. Standardization of cognitive and psychosocial outcome measures is essential.

Background and objective: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline, oxidative stress, and mitochondrial dysfunction. Fibroblast growth factor 21 (FGF21) has demonstrated neuroprotective effects, though its role in AD pathogenesis remains unclear. The present study aims to discover neuroprotective effects of FGF21 in AD by examining its influence on energy metabolism and neuronal survival through the PI3K/Akt signaling pathways.

Methods: In vivo experiments were performed using 5×FAD transgenic mice, while in vitro assays utilized amyloid beta 1-42 (Aβ1-42)-treated SH-SY5Y cells and a co-culture system of primary rat astrocytes with SH-SY5Y cells. To evaluate the effects of FGF21 modulation, we performed both gain- and loss-of-function experiments and assessed outcomes using behavioral testing, histopathological and ultrastructural analyses, oxidative stress and mitochondrial function assays, and Western blotting. The involvement of the PI3K/Akt/mTOR pathway was explored using the PI3K inhibitor LY294002.

Results: Both in vivo and in vitro AD models exhibited reduced FGF21 expression. FGF21 downregulation impaired PI3K/Akt signaling, induced neuronal apoptosis, and disrupted metabolic homeostasis. Loss of FGF21 resulted in cognitive and metabolic dysfunction in AD mice. Conversely, FGF21 overexpression activated PI3K/Akt signaling, suppressed neuronal apoptosis, and restored metabolic functions in AD models.

Conclusion: FGF21 alleviates AD-related cognitive impairment and restores metabolic function by activating the PI3K/Akt pathway.

Objective: To investigate the association between thrombin-activatable fibrinolysis inhibitor (TAFI) genetic polymorphisms and therapeutic efficacy in spontaneous intracerebral hemorrhage (ICH) patients treated with intra-hematoma rt-PA thrombolysis.

Methods: This retrospective exploratory study analyzed 59 ICH patients who underwent intra-hematoma rt-PA thrombolysis. TAFI polymorphism genotyping was performed using PCR-RFLP. Primary outcomes included radiological efficacy, functional outcomes (mRS ≤3), and mortality.

Results: Genetic analysis was completed in 55 patients. Genotype distribution: Ile325Ile 28 (47.5%), Thr325Ile 25 (42.4%), Thr325Thr 2 (3.4%), consistent with Hardy-Weinberg equilibrium (P=0.35). The Ile325Ile group showed a trend toward better functional outcomes compared to Thr325Ile (25.0% vs 8.0%, OR=3.83, P=0.108), but had significantly higher mortality (14.3% vs 0%, P=0.042). Multivariate analysis identified age (OR=0.948, P=0.024) and admission NIHSS score (OR=0.908, P=0.021) as independent predictors of good functional outcomes; TAFI genotype was not retained as an independent predictor (P=0.138).

Conclusions: This exploratory study provides preliminary evidence that TAFI genetic polymorphisms may be associated with differential responses to intra-hematoma rt-PA thrombolysis, with potential genotype-dependent dissociation between radiological and functional outcomes. These findings require validation in larger studies.

Objective: To evaluate remission, recurrence, and complication rates following endoscopic transsphenoidal surgery (ETSS) for Cushing disease (CD) at a Canadian tertiary center, and assess concordance of preoperative cerebral MRI and inferior petrosal sinus sampling (IPSS) with intraoperative adenoma laterality.

Methods: We retrospectively reviewed 92 patients with confirmed CD who underwent ETSS by a single neurosurgeon between August 2007 and May 2025. Outcomes included biochemical remission, recurrence, and complications. We assessed the concordance of preoperative MRI and IPSS with intraoperative tumor localization.

Results: The cohort included 92 patients (mean age 46.6 ± 15.0 years; 77% female) with a median follow-up of 18.3 months (IQR 6.4-44.9). Preoperative MRI identified a microadenoma in 63 cases, macroadenoma in 17, and was negative in 12. Remission was achieved in 76.7% (86.4% early ≤6 months), with 7.9% experiencing recurrence after a median of 13.2 months. Complications included arginine vasopressin deficiency (AVPD) in 43.5% of the cohort (persistent >6 months in 10.2%), hypothyroidism in 14.1%, syndrome of inappropriate antidiuretic hormone secretion (SIADH) in 5.4%, and cerebrospinal fluid (CSF) leak in 3.3%. Intraoperatively, 78.8% of microadenomas were in the posterior adenohypophysis, and 27.4% exhibited multifocal distribution. Concordance of adenoma laterality was 56.5% for MRI and 41.7% for IPSS, with no statistically significant difference.

Conclusion: ETSS achieved high remission with low morbidity in CD. Frequent posterior and multifocal adenomas in the adenohypophysis support systematic pituitary exploration. Localization remains challenging, with limited concordance using MRI and IPSS, highlighting the need for cautious interpretation in surgical planning.

Background: Traumatic brain injury (TBI) triggers secondary neuronal damage via oxidative stress and ferroptosis. This study examines the neuroprotective effect of fibroblast growth factor 21 (FGF21) in TBI and its regulation of the Nrf2/GPX4 signaling pathway.

Methods: TBI was induced in C57BL/6 mice using a controlled cortical impact model. Post-injury, mice received low- or high-dose recombinant FGF21, with or without the Nrf2 inhibitor ML385. Neurological function was evaluated using Garcia scoring and the Morris Water Maze. Oxidative stress, cerebral edema, and iron deposition were measured. In vitro, primary rat cortical neurons were treated with erastin (a ferroptosis inducer) ± FGF21 or ferrostatin-1. Neuronal viability, morphology, and Nrf2/GPX4 expression were analyzed by immunofluorescence, Western blotting, and RT-qPCR.

Results: FGF21 significantly improved neurological outcomes in TBI mice, reduced edema and iron deposition, and attenuated oxidative stress. In vitro, FGF21 preserved neuronal structure and viability under ferroptotic conditions. Mechanistically, it enhanced Nrf2 nuclear translocation and upregulated GPX4. These effects were abolished by Nrf2 inhibition, confirming pathway involvement.

Conclusion: FGF21 protects against TBI-induced secondary injury by suppressing ferroptosis and oxidative stress via Nrf2/GPX4 activation, highlighting its potential as a therapeutic strategy for TBI.

Objective: This study aims to investigate the association of clinical characteristics, vascular morphological features, and hemodynamic parameters with rupture risk in anterior communicating artery (ACoA) aneurysms.

Methods: A retrospective analysis was conducted on 293 patients with ACoA aneurysms, categorized into ruptured and unruptured groups. Clinical data, vascular morphological parameters, and hemodynamic variables were compared between groups. Binary logistic regression analysis was used to identify independent predictors of aneurysm rupture.

Results: Statistically significant differences were observed between the ruptured and unruptured groups in terms of sex, smoking status, systolic and diastolic blood pressure at admission, curvature of the affected A1 segment, spatial angle between the affected internal carotid artery and ipsilateral A1 segment, and the curvature length of the A1 segment. Hemodynamic parameters, including wall shear stress (WSS) and the presence of blood flow vortices, were notably elevated in ruptured aneurysms. Binary logistic regression analysis identified the curvature of the affected A1 segment (odds ratio [OR] = 0.001, 95% confidence interval [CI]: 0.000-0.173, p = 0.010), the angle between the affected A1 and A2 segments (OR = 0.963, 95% CI: 0.933-0.994, p = 0.020), and WSS on the affected side (OR = 0.140, 95% CI: 0.072-0.269, p < 0.001) as significant independent indicators of rupture risk.

Conclusion: Among patients with ACoA aneurysms, increased curvature of the A1 segment and elevated WSS on the affected side were the most robust predictors of rupture. These parameters remained significant across both univariate and multivariate analyses, underscoring their potential utility in clinical risk stratification.

Background/objective: Trigeminal neuralgia (TN) causes disabling facial pain often refractory to medication. Microvascular decompression (MVD) and percutaneous balloon compression (PBC) are established surgical options, yet their comparative efficacy and safety remain debated.

Methods: Following PRISMA guidelines, a systematic review and meta-analysis of 19 double-arm studies (2,674 patients; 1486 MVD, 1188 PBC) was performed. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were computed. Evidence certainty was graded via GRADE.

Results: MVD and PBC achieved similar initial complete pain relief (RR = 1.01, 95% CI 0.98-1.05, p = 0.49) and adequate relief (RR = 1.00, 95% CI 0.97-1.02, p = 0.67). Long-term complete (RR = 1.11, 95% CI 0.97-1.27, p = 0.13) and adequate relief (RR = 1.06, 95% CI 0.97-1.15, p = 0.17) were likewise equivalent. Pain recurrence modestly favored MVD (RR = 0.72, 95% CI 0.51-1.00, p = 0.05), while permanent complications did not differ (RR = 1.09, 95% CI 0.43-2.75, p = 0.86). Leave-one-out analyses confirmed robustness, and Egger's tests showed no publication bias. GRADE rated certainty high for initial relief, moderate for long-term outcomes and recurrence, and low for complications.

Conclusion: MVD and PBC yield equivalent short-term and long-term pain relief, as well as similar safety, in TN. MVD may offer slightly lower recurrence, whereas PBC remains advantageous for elderly or medically fragile patients. These data support the use of tailored surgical selection guided by patient comorbidity and durability expectations.

Background and purpose: Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) detection technique was used to screen stroke susceptibility gene methyltetrahydrofolate reductase (MTHFR), Shandong Province, to evaluate its predictive effect and clinical application value for stroke.

Methods: Sanger sequencing of MTHFR-C677T (rs 1,801,133) and A1298C (rs 1,801,131) was performed on blood samples of 635 patients with high-risk stroke, and the mutation of A1298C was detected by CRISPR. Based on the two sequencing results and the incidence of stroke, the predictive effect of MTHFR gene detection and the clinical application value of CRISPR technology were verified.

Results: Sanger sequencing revealed a statistically significant difference (p < 0.05) in MTHFR C677T mutation frequency between the stroke group and controls, and between the high-risk group and controls, indicating an association of C677T polymorphism with stroke risk. Comparison between CRISPR and Sanger results showed similar mutation detection rates across groups (26.9% vs. 26.5% in stroke/TIA/high-risk groups; both 32.6% in controls). CRISPR demonstrated 97.6% sensitivity, 98.5% specificity, 98.3% concordance, and a Kappa value of 0.956. Furthermore, homocysteine level analysis indicated significant differences (p < 0.05) in MTHFR C677T and A1298C polymorphisms between individuals with normal and high homocysteine (HHcy) in stroke‑related groups.

Conclusion: CRISPR detection technique has high accuracy and is suitable for clinical application. The increase of homocysteine level may be one of the risk factors of stroke.