Background: Dementia is a major public health challenge for aging societies worldwide. Neuroinflammation is thought to be a key factor in dementia development. The aim of this study was to comprehensively assess translocator protein (TSPO) expression by positron emission tomography (PET) imaging to reveal the characteristics of neuroinflammation in dementia. Methods: We used a meta-analysis to retrieve literature on TSPO expression in dementia using PET imaging technology, including but not limited to the quality of the study design, sample size, and the type of TSPO ligand used in the study. For the included studies, we extracted key data, including TSPO expression levels, clinical characteristics of the study participants, and specific information on brain regions. Meta-analysis was performed using R software to assess the relationship between TSPO expression and dementia. Results: After screening, 12 studies that met the criteria were included. The results of the meta-analysis showed that the expression level of TSPO was significantly elevated in patients with dementia, especially in the hippocampal region. The OR in the hippocampus was 1.50 with a 95% CI of 1.09 to 1.25, indicating a significant increase in the expression of TSPO in this region compared to controls. Elevated levels of inflammation in the prefrontal lobe and cingulate gyrus are associated with cognitive impairment in patients. This was despite an OR of 1.00 in the anterior cingulate gyrus, indicating that TSPO expression in this region did not correlate significantly with the findings. The overall heterogeneity test showed I² = 51%, indicating moderate heterogeneity. Conclusion: This study summarizes the existing literature on TSPO expression in specific regions of the brain in patients with dementia, and also provides some preliminary evidence on the possible association between neuroinflammation and dementia. However, the heterogeneity of results and limitations of the study suggest that we need to interpret these findings with caution. Future studies need to adopt a more rigorous and consistent methodological design to more accurately assess the role of neuroinflammation in dementia, thereby providing a more reliable evidence base for understanding pathological mechanisms and developing potential therapeutic strategies.

Objective: In this study, clinical data from vestibular migraine (VM) patients and healthy control populations were collected to analyze the clinical data of VM patients, especially the history of motion sickness, and to understand their clinical characteristics.Methods: According to VM diagnostic criteria, 140 patients diagnosed with confirmed VM (cVM) and probable VM (pVM) who attended the outpatient and inpatient ward of Jiaxing First Hospital between August 2017 and June 2021, as well as 287 healthy check-ups in the health management center, were analyzed and compared in terms of age, gender, and previous history of motion sickness.Results: A comparison of clinical data related to VM patients and the control population showed that there were more women in the VM group (P < 0.01) and that patients in the VM group were older (P < 0.05) and had a higher prevalence of history of motion sickness history (P < 0.01). Analysis after matching gender and age revealed that patients in the cVM group were older than those in the pVM group (P < 0.05), but the proportion of motion sickness was lower than in the pVM group (P < 0.05). The age of the patients in the cVM group was mainly distributed around 50 years of age, following a normal distribution, whereas the age distribution of the patients in the pVM group did not have a significant trend of age concentration and was distributed at all ages.Conclusion: The history of motion sickness is significant in patients with VM and may be a potential suggestive factor for the diagnosis of VM.

Chronic cerebral hypoperfusion (CCH) is a significant contributor to vascular cognitive impairment (VCI), often linked to cortical and hippocampal damage. This study investigates the therapeutic potential of salidroside (SLDS) in mitigating CCH-induced brain injury by modulating microglial activation and inflammatory responses. We established a CCH model in mice using the 0.16/0.18 mm bilateral common carotid artery stenosis (BCAS) procedure. We assessed cerebral blood flow (CBF) via laser speckle contrast imaging, while neuropathology was evaluated through Nissl staining and immunofluorescence (IF) experiments. Cognitive deficits were measured using the Morris water maze test. Neuronal apoptosis and neuroinflammation were examined through IF, ELISA, and qRT-PCR. BCAS-induced hypoperfusion resulted in a marked reduction in CBF, increased neuronal apoptosis, and significant cognitive deficits. SLDS treatment effectively countered these effects by shifting microglial polarization from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype, reducing pro-inflammatory cytokine levels, and enhancing neuronal survival. SLDS demonstrates strong neuroprotective potential against CCH-induced brain injury by reducing inflammation and preventing neuronal apoptosis. These findings highlight the promise of SLDS as a therapeutic agent for chronic cerebrovascular disorders, warranting further investigation into its molecular mechanisms and clinical applicability.

Background: Ischemic stroke associated with atherosclerosis is globally named atherothrombotic stroke. Presently, the underlying pathogenic genes promoting carotid atherosclerotic plaques transfer from a stable to unstable state remains elusive. This study aims to find the hub genes disturbing the stability of plaques and explore the primary cells affected by these hub genes. Methods: The optimal hub genes from five datasets for unstable plaques were identified by overlapping genes derived from Boruta and LASSO algorithms. The hub genes’ expression levels in stroke patients were confirmed through RT-qPCR. Visualization of the hub genes’ expression across various cell clusters was achieved with the aid of the Seurat R package. Then, hub genes were overexpressed or knock-down by lentivirus and siRNA, respectively. The inflammatory factors in the culture medium were detected using an ELISA assay. Results: Eight genes (APOD, ASXL1, COL4A5, HTR7, INF2, NSUN6, PDSS2, and RBBP7) were identified and confirmed by RT-qPCR. The prognostic model was built upon this eight-gene composite foundation, and the area under the curve was 0.98. Based on CIBERSORT findings, unstable plaques displayed a higher macrophage proportion compared to stable ones (P < 0.05). These eight genes also correlated with infiltrated immune cells, especially macrophages. Then, according to single-cell RNA-seq analysis, we found that the eight hub genes mainly expressed in macrophages. The cellular localization of two hub genes (NSUN6 and HTR7) with high distinguishability was confirmed, and gene set enrichment analysis also clarified the possible biological pathways regulated by them. The findings from the in vitro investigation revealed that TNF-α and IL-6 were reduced in macrophages with NSUN6 overexpression or HTR7 knockdown. Conclusion: Eight hub genes, especially NSUN6 and HTR7, were found to promote the progression of plaques by regulating the immune responses of macrophages.

This study was aimed to investigate the relationship between neuron-specific enolase (NSE) and swallowing dysfunction in patients with acute ischemic stroke (AIS) and evaluate the impact of early enteral nutrition intervention on NSE levels. A retrospective study was conducted involving 445 AIS patients admitted to the neurology department of the Affiliated Hospital of Jiaxing University between September 2015 and August 2022. Data collected included gender, age, water-swallowing test (WST) score upon admission, and NSE examination results on admission, the 5th day, and the 10th day. Among 445 enrolled AIS patients, 42.0% (187/445) exhibited swallowing dysfunction. Key findings revealed: (1) Positive correlation between WST severity and serum NSE levels across all timepoints (P < 0.05). (2) Dysphagia patients demonstrated elevated NSE levels versus controls (P < 0.05). (3) Early enteral nutrition intervention (n = 98) significantly reduced NSE levels by day 10 compared to non-intervention group (P < 0.05), though no intergroup differences were observed at admission or day 5 (P > 0.05). NSE measurement is a simple supplement to the WST. There existed a significant correlation between NSE and swallowing dysfunction, making NSE a potential preliminary screening indicator for evaluating in ischemic stroke patients. And early implementation of enteral nutrition intervention could effectively reduce NSE levels in patients with ischemic stroke.

Background: Horizontal semicircular canal benign paroxysmal positional vertigo(HSC-BPPV) is the second most common type of BPPV. It is difficult to diagnose and treat, which has a serious impact on the prognosis of patients. Objectives: To study the clinical features of HSC-BPPV and the influencing factors of residual dizziness (RD). Materials and methods: The clinical data of 358 patients with BPPV were retrospectively collected. The differences between HSC-BPPV and posterior semicircular canal benign paroxysmal positional vertigo (PSC-BPPV) were compared, and the influencing factors of RD after HSC-BPPV repositioning were analyzed. Results: (1) Compared with PSC-BPPV, HSC-BPPV had a lower success rate of first repositioning (64.7 vs. 75.0%), a higher incidence of RD (57.3 vs. 43.8%), and a higher DHI score (40.0 vs. 34.0), and the differences were statistically significant (p < .05). (2) Logistic regression analysis showed that age >= 60 years, secondary, DHI score, successful first repositioning were the influencing factors for the development of RD after HSC-BPPV repositioning (p < .05). Conclusions and significance: The diagnosis and treatment of HSC-BPPV is difficult, and RD is prone to occur. Clinicians need to strengthen the training of HSC-BPPV diagnosis and treatment to reduce the occurrence and progression of RD.