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.

Objectives This study aims to evaluate and compare the clinical differences in intravenous thrombolytic therapy among patients with cerebral infarction transported to the hospital by private cars versus ambulances in Jiaxing, a non-supersized city in China. It also sought to examine the impact of different transportation methods on emergency department arrival times, delays in initiating thrombolytic therapy and final clinical prognosis. The findings aim to provide a basis for optimising emergency treatment protocols and improving outcomes for patients with cerebral infarction. Design Data on age, gender, height, weight, body mass index, season, time of day (day vs night), modified Rankin Scale scores, door-to-needle time (DNT) and onset-to-needle time (ONT) were retrospectively collected from 808 patients admitted to the emergency department of the Affiliated Hospital of Jiaxing University for intravenous thrombolysis between January 2019 and September 2022. The data were analysed and compared. Setting A retrospective cohort study conducted in Jiaxing, China. Outcome measures The primary outcomes were DNT and ONT. Results Among the 808 eligible patients, 279 (34.53%) were transported by ambulance, and 529 (65.47%) arrived by private car. Patients in the private car group were younger on average than those in the ambulance group (aged 64.70 vs 68.41 years). Although ambulance transport resulted in shorter prehospital transportation times (113.89 vs 127.38 min), patients arriving by private car had shorter thrombolytic therapy initiation times (39.90 vs 36.30 min). At admission, the National Institutes of Health Stroke Scale scores were higher in the ambulance group (4 vs 2), indicating more severe conditions and a greater proportion of patients requiring bridging thrombectomy after thrombolysis (7.53% vs 3.02%). Conclusion In non-supersized cities, private car transportation for acute patients with cerebral infarction may lead to shorter DNT and ONT compared with those in ambulance transport. However, patients transported by ambulance tended to have more severe conditions, highlighting the importance of tailored emergency response strategies.

BACKGROUND Small cell lung cancer (SCLC) is the most malignant type of lung cancer. Even in the latent period and early stage of the tumor, SCLC is prone to produce distant metastases with complex and diverse clinical manifestations. SCLC is most closely related to paraneoplastic syndrome, and some cases present as paraneoplastic peripheral neuropathy (PPN). PPN in SCLC appears early, lacks specificity, and often occurs before diagnosis of the primary tumor. It is easy to be misdiagnosed as a primary disease of the nervous system, leading to missed diagnosis and delayed diagnosis and treatment. CASE SUMMARY This paper reports two cases of SCLC with limb weakness as the first symptom. The first symptoms of one patient were rash, limb weakness, and abnormal electromyography. The patient was repeatedly referred to the hospital for limb weakness and rash for > 1 year, during which time, treatment with hormones and immunosuppressants did not lead to significant improvement, and the condition gradually aggravated. The patient was later diagnosed with SCLC, and the dyskinesia did not worsen as the dermatomyositis improved after antineoplastic and hormone therapy. The second case presented with limb numbness and weakness as the first symptom, but the patient did not pay attention to it. Later, the patient was diagnosed with SCLC after facial edema caused by tumor thrombus invading the vein. However, he was diagnosed with extensive SCLC and died 1 year after diagnosis. CONCLUSION The two cases had PPN and abnormal electromyography, highlighting its correlation with early clinical indicators of SCLC.

Periodic paralysis (PP) is a group of ion channel diseases with incomplete autosomal dominant inheritance, except in sporadic patients. Ion channel gene mutations cause transient abnormalities in skeletal muscle excitability and muscle weakness. Different mutation sites cause different pathogenesis, which is very important for the classification, clinical manifestations, treatment and prognosis of periodic paralysis. Currently, the recognized mutated genes are CACNA1S (chromosome 1q31-32), SCN4A (chromosome 17q23-25), KCNJ2 (chromosome 17q23), and KCNJ18 (chromosome 17p11.2). The common mutation sites include R528H and R1239H in CACNA1S , and R672H and T704M in SCN4A . However, there is accumulating evidence that other mutation sites in CACNA1S and SCN4A , and even new ion channel mutations may induce periodic paralysis. Their different pathogenesis, clinical features and therapeutic measures have been widely described. This review will introduce the clinical manifestations of periodic paralysis, the different mutation sites of each ion channel, and the pathogenesis. Based on the clinical types of periodic paralysis, the characteristics of the latter are further discussed.

Ischemic stroke, a leading cause of neurological morbidity, is characterized by extensive neuronal injury and a robust inflammatory response. Erbin, a scaffold protein involved in multiple cellular signaling pathways, regulates neuroinflammation and may confer neuroprotection against ischemia–reperfusion (I/R) injury. A mouse model of middle cerebral artery occlusion was utilized to evaluate the neuroprotective role of Erbin. Male mice were allocated into groups receiving either a lentiviral (LV) control vector or LV-mediated Erbin overexpression, followed by I/R injury induction. Neurological function, infarct volume, and expression levels of inflammatory cytokines and mitogen-activated protein kinase (MAPK) signaling proteins were analyzed. Overexpression of Erbin via LV transduction significantly reduced cerebral infarct volume and mitigated neurological impairments post-I/R injury. Furthermore, Erbin overexpression suppressed the phosphorylation of p38 and extracellular signal-regulated kinase in HT22 neuronal cells, indicating attenuation of MAPK pathway activation. Notably, Erbin overexpression modulated the inflammatory response elicited by I/R injury, leading to a reduction in proinflammatory cytokine levels.