Behavioural Neurology最新文献

It is well-established that light therapy can alleviate cognitive impairment, and ambient illumination (AI) can quantify the amount of exposure to light. However, the relationship between AI and cognitive impairment has been largely understudied. Objectives. We aimed to examine the cross-sectional associations between AI and impaired cognition using data from the National Health and Nutrition Examination Survey (NHANES) (2011-2013) database. Methods. The correlation between AI and cognitive impairment was analyzed using multivariate logistic regression models. Nonlinear correlations were explored using curve fitting. Results. Multivariate logistic regression yielded an OR of 0.872 (95% CI 0.699, 1.088) for the association between AI and cognitive impairment after adjusting for covariates. Smooth curve fitting showed that the correlation was nonlinear, with an inflection point at 1.22. Conclusions. These results suggested that the level of AI may be linked to cognitive impairment. We found a nonlinear relationship of AI with cognitive impairment.

The early introduction of a low phenylalanine (Phe) diet has been demonstrated to be the most successful treatment in subjects with phenylketonuria (PKU), especially for preventing severe cognitive and neurological damages. However, it still concerns that even if treated in the first months of life with supplements and following a diet, they can show slight scores below people without PKU in neuropsychological assignments. We investigated 20 adults with classical PKU aged 19-48 years (mean age 29 years) and 20 heathy controls matched by age, gender, and years of education. Patients and controls were assessed with an extended neuropsychological battery, as well as psychological aspects and quality of life, also the last Phe level result was obtained. Results showed that the most affected cognitive domains are processing speed, executive functioning, memory, and also theory of mind, but very well-preserved verbal fluency, language, and visuospatial functioning. In quality of life, some significant results were seen specially in anxiety of Phe levels, anxiety of Phe levels during pregnancy, guilt if poor adherence to supplements, and if dietary protein restriction not followed. No significant results were obtained for the psychological variables. In conclusion, it has been shown that a combination of a low Phe diet, supplement intake, and keeping Phe levels in a low range seems appropriate to have the most normal and alike cognitive performance to persons without PKU.

[This retracts the article DOI: 10.1155/2021/2560388.].

[This retracts the article DOI: 10.1155/2022/2032093.].

Alzheimer's disease (AD) is the most common form of dementia and a significant social and economic burden. Estrogens can exert neuroprotective effects and may contribute to the prevention, attenuation, or even delay in the onset of AD; however, long-term estrogen therapy is associated with harmful side effects. Thus, estrogen alternatives are of interest for countering AD. Naringin, a phytoestrogen, is a key active ingredient in the traditional Chinese medicine Drynaria. Naringin is known to protect against nerve injury induced by amyloid beta-protein (Aβ) _25-35, but the underlying mechanisms of this protection are unclear. To investigate the mechanisms of naringin neuroprotection, we observed the protective effect on Aβ _25-35-injured C57BL/6J mice's learning and memory ability and hippocampal neurons. Then, an Aβ _25-35 injury model was established with adrenal phaeochromocytoma (PC12) cells. We examined the effect of naringin treatment on Aβ _25-35-injured PC12 cells and its relationship with estrogen receptor (ER), phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), and glycogen synthase kinase (GSK)-3β signaling pathways. Estradiol (E₂) was used as a positive control for neuroprotection. Naringin treatment resulted in improved learning and memory ability, the morphology of hippocampal neurons, increased cell viability, and reduced apoptosis. We next examined the expression of ERβ, p-AKT (Ser473, Thr308), AKT, p-GSK-3β (Ser9), GSK-3β, p-Tau (Thr231, Ser396), and Tau in PC12 cells treated with Aβ _25-35 and either naringin or E₂, with and without inhibitors of the ER, PI3K/AKT, and GSK-3β pathways. Our results demonstrated that naringin inhibits Aβ _25-35-induced Tau hyperphosphorylation by modulating the ER, PI3K/AKT, and GSK-3β signaling pathways. Furthermore, the neuroprotective effects of naringin were comparable to those of E₂ in all treatment groups. Thus, our results have furthered our understanding of naringin's neuroprotective mechanisms and indicate that naringin may comprise a viable alternative to estrogen therapy.

Glioblastoma (GBM) is a highly malignant cancer, the prognosis of which is pretty poor. Long non-coding RNAs (lncRNAs) are a class of non-coding RNAs, which play important roles in carcinogenesis process of many cancers including GBM. In this study, we want to clarify the expression, biological function, and molecular mechanism of lncRNA KTN1 antisense RNA 1 (KTN1-AS1) in GBM tumor progression. We found that KTN1-AS1 expression was upregulated in GBM tissues and cell lines. KTN1-AS1 played oncogenic roles to facilitate proliferation, migration, and invasion of GBM cells. Then, we revealed that miR-505 was a target of KTN1-AS1, and its expression was decreased in GBM. KTN1-AS1 contributed to GBM progression by mediating miR-505. Finally, we demonstrated that KTN1-AS1 upregulated some target oncogenes of miR-505 including ZEB2, HMGB1, and RUNX2 in GBM cells. All in all, we concluded that the highly expressed KTN1-AS1 in GBM played oncogenic roles to facilitate GBM progression by targeting miR-505.

[This retracts the article DOI: 10.1155/2021/9731519.].

Alzheimer's disease (AD), as the main cause of dementia, has a progressive and neurodegenerative pattern with number of cases increasing over the next decades. Therefore, discovering an effective treatment with the ability to invert memory impairment and pathophysiological events of AD seems to be required. The present study performed to investigate the probable effects of Edaravone (EDV) in AD-like disorder induced by intracerebroventricular streptozotocin (ICV-STZ) administration in mice. This study also compares the two different methods of ICV-STZ in the memory impairment induction. NMRI male mice were administrated with 3 mg/kg of STZ for two times during 48 hours span, and after 24 hours, animals were treated with EDV (5 and 10 mg/kg), Donepezil, and Memantine for 14 days. After behavioral tests regarding memory and cognitive function, animals were sacrificed, and the hippocampi were utilized for further analyses. Our results demonstrated that administration of STZ induced memory impairment in the Morris water maze (MWM) test and decreased the discriminative factor in novel object recognition (NOR). The biochemical output shows a significant decrease in ferric reducing antioxidant power (FRAP) and glutathione (GSH) levels followed by increase in malondialdehyde (MDA) and protein carbonylation (PCO) levels. The output showed no difference between the patterns of AD-like disorder induction. Following our treatment groups, administration of EDV (5 and 10 mg/kg), Donepezil, and Memantine significantly improved memory performance and discriminatory behavior. Aforementioned treatments managed to improve FRAP and GSH content of hippocampus, while significantly attenuating MDA, PCO, and nitric oxide overproduction. In addition, no significant difference has been observed between the effect of 5 and 10 mg/kg EDV application. It was supposed that EDV managed to ameliorate memory dysfunction, discriminatory behavior, oxidative stress, and cellular antioxidant power in a dose-independent pattern in mice.

Objective: To analyse the clinical efficacy of acupuncture and routine treatment in improving dystonia in children with cerebral palsy.

Method: The randomized controlled trials published from the establishment of the databases to August 2022 on acupuncture in the treatment of dystonia in children with cerebral palsy were collected and comprehensively searched in China national knowledge infrastructure (CNKI), weipu (VIP), Wanfang, SinoMed, PubMed, Excerpta medica database (EMBASE), and Cochrane Library. The literature was selected according to the established standards, the quality of the included studies was evaluated, the heterogeneity of the included studies was evaluated with the I² test, and the appropriate model was selected for analysis. Sensitivity analysis was used to evaluate the reliability of the results, and a funnel plot was used to evaluate the publication bias.

Results: Fifteen studies were included in the meta-analysis. The control group was treated with routine treatment and acupuncture combined with routine treatment. The outcome index showed that the effect in the treatment group was better: Modified Ashworth Scale score: -0.52, 95% confidence interval (CI) (-0.62 to -0.41), p < 0.01. The treatment group showed reduced muscle tension to a greater extent (integral eletromyographic (iEMG) score: standard mean square deviation = -2.97, 95% CI (-4.87 to -1.06), p < 0.01). The effective rate in the control group was 74.2% and that in the treatment group was 91.5%, odds ratio = 3.70, 95% CI (2.02-6.78), p < 0.01. The funnel plot showed publication bias.

Conclusion: Acupuncture combined with routine training could improve muscle tension abnormalities and improve the efficiency of clinical treatment.

Vitamin B6 (VB₆) exhibits therapeutic effects towards autism spectrum disorder (ASD), but its specific mechanism is poorly understood. Rat dams were treated with VB₆ standard, VB₆ deficiency, or VB₆ supplementary diet, and the same treatment was provided to their offspring, with their body weights monitored. Three-chambered social test and open field test were employed to evaluate the effect of VB₆ on autism-like behaviors. Gamma-aminobutyric acid (GABA) generation and synaptic inhibition of neurons in the hippocampus of rat were detected via immunofluorescence staining, followed by the measurement of GABA concentration through high-performance liquid chromatography (HPLC). The role of VB₆ in the autophagy and apoptosis of cells was determined via Western blot and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). In order to conduct rescue experiments, the inhibition of mammalian target of rapamycin (mTOR) or the activation of GABA was achieved by drug administration to the offspring rats with VB₆ deficiency. As a result, no evident difference in weight was observed in the offspring with varied VB₆ treatments. VB₆ deficiency impaired social interaction; aggravated self-grooming and bowel frequency; decreased GABA concentration, VIAAT, GAD67, vGAT expressions, and LC3 II/LC3 I ratio; increased p62 level and p-mTOR/mTOR ratio; and promoted cell apoptosis. Inhibition of mTOR reversed the effect of VB₆ deficiency on cell autophagy. GABA activation or mTOR inhibition offset the role of VB₆ deficiency in autism-like behaviors and hippocampal GABA expression. Collectively, VB₆ deficiency induces autism-like behaviors in rats by regulating mTOR-mediated autophagy in the hippocampus.