Objective: To evaluate the state of evidence for the beneficial and harmful effects of Tai Chi on non-motor disorders in post-stroke patients. Design: Systematic review and meta-analysis of published studies. Subjects: Stroke survivors who received conventional rehabilitation therapy or Tai Chi training. Data sources: We searched seven electronic literature databases and one clinical registry platform to collect data from randomized controlled trials published up to July 26, 2020. Results: A total of 11 randomized controlled trials with 723 stroke survivors met the inclusion criteria, of which six were included in the meta-analysis. Among the 11 studies, one was assessed as “low”, eight were assessed as “moderate”, and only two were assessed as “high” for the assessment of methodologic quality. Compared to patients who received conventional rehabilitation therapy, those who received Tai Chi training showed greater improvement in scores of depression (standardized mean difference (SMD) [95% confidence interval (CI)] = 0.36 [0.10, 0.61], Grading of Recommendations Assessment, Development, and Evaluation [GRADE]: very low). There were no differences in the improvements in post-stroke global mental disorders (mean difference (MD [95% CI] = 6.15 [−3.05, 15.36], GRADE: moderate) or sleep disorders (MD [95% CI] = 0.33 [−1.51, 1.81], GRADE: low) between Tai Chi and control groups. Conclusion: Tai Chi may alleviate post-stroke depression in stroke survivors but has no clear effects on post-stroke cognitive and sleep disorders.

Introduction: Uric acid (UA) is considered as a potential risk factor for coronary heart disease (CHD) and other cardiovascular diseases (CVDs). However, the association between hyperuricemia and the risk of CHD and other cardiovascular outcomes has not been fully clarified. This systematic review and dose-response meta-analysis was conducted to comprehensively the association between hyperuricemia and the risk of CHD or other cardiovascular outcomes in the general population. Methods: We systematically searched Medline, Cochrane Library, Embase, and two clinical trial registration databases from inception to June 30, 2025, without restrictions on language or publication status. Only cohort and case-control studies enrolling participants without CHD, other CVDs, or gout at baseline were included. The primary outcome was the association between hyperuricemia and the risk of CHD, and secondary outcomes were the association between hyperuricemia and the risk of fatal and nonfatal CVDs, included CHD death, CVD, CVD death, and myocardial infarction (MI). Risk of bias was assessed using the Risk Of Bias In Non-randomized Studies-of Exposure (ROBINS-E) tool. All statistical analyses were performed using R 4.4.2. We conducted meta-analyses, heterogeneity assessments, publication bias tests, trim-and-fill analyses, subgroup and sensitivity analyses, meta-regressions, and dose-response meta-analyses. The GRADE recommendation was used to evaluate the quality of evidence. Results: A total of 42 articles representing 39 individual studies and 1,082,880 participants were included. Among these, 2 articles were assess as “very high risk of bias”, eight as “high risk of bias”, and two as “some concerns”. Hyperuricemia was significantly associated with an increased risk of CHD [HR 1.21 (95%CI 1.14–1.28), p < 0.001, I2 = 34.34%], CHD death [1.20 (1.05–1.36), p = 0.005, I2 = 41.28%], CVD death [1.75 (1.12–2.74), p = 0.014, I2 = 49.48%], and MI [1.23 (1.03–1.47), p = 0.025, I2 = 56.96%]. No significant association was observed for overall CVD risk [1.09 (0.94–1.27), p = 0.245, I2 = 0%]. For each unit increase in serum UA, the risk of CHD, CHD death, CVD, CVD death, and MI increased by 16%, 13%, 12%, 11%, and 7%, respectively. No factors with a significant impact on the results were identified through subgroup analyses or meta-regression. Sex may have a potential influence, but the results were not robust. Further dose-response meta-analysis revealed a linear relationship between higher serum UA and CVD risk, and a U-shaped association between serum UA and CVD mortality in men. The quality of evidence was rated as low for CHD and very low for the other cardiovascular outcomes. Conclusion: This systematic review and dose-response meta-analysis provides low- to very-low-quality evidence suggesting that hyperuricemia may be associated with an increased risk of CHD and other fatal or nonfatal CVDs. Trial registration: This study was registered in PROSPERO CRD42024538553.

Background: Alzheimer’s disease is a neurodegenerative disease characterized by progressive cognitive decline and dysfunction of independent living ability, with huge economic and healthy burden worldwide. However, there is still a lack of effective long-term drugs to improve cognitive function and reduce or halt disease progression. Phase III clinical trials of anti-AD drugs based on different hypotheses were in the pipeline, and this protocol for a systematic review and meta-analysis aims to determine what is the most effective direction for the development of drugs on cognitive improvement.Methods/design: We will search the following literature databases for eligible studies from inception to December 2021: Ovid MEDLINE, Ovid Embase, PubMed MEDLINE, and Cochrane Central Register of Controlled Trials. Google Scholar,ClinicalTrials.govregistration platform, and the AlzForum website will also be searched for additional studies. Studies will be included irrespective of publication status or language. Phase III clinical trials reporting on the effect of anti-AD drugs on participants with AD will be included. Two independent reviewers will screen the hit articles and identify phase III clinical trials, extract data, and assess the quality of each study individually. The Cochrane Risk of Bias tool 2 (RoB 2) will be used to assess the risk of bias. For each kind of drugs based on the corresponding hypothesis, we will compare the study design and demographic features of the clinical trials and include appropriate studies in the network meta-analysis. The primary outcomes will be the indicators of cognitive improvement. The secondary outcomes will be activities of daily living, neuroimaging changes, biomarkers, and safety. Through network meta-analysis, we will suggest the hypothesis that most likely to improve cognitive function and provide the ranks of all kinds of drugs. We will give recommendation grade of each comparison using the Confidence In Network Meta-Analysis (CINeMa) tool.Discussion: This study will provide helpful evidence for further drug development and clinical practice for treating Alzheimer’s disease.Systematic review registration: PROSPEROCRD42021251507

Background: Most of the FDA approved drugs for AD are symptom driven and effects are limited. Because AD is a complex disease involving multiple pathological changes, such as senile plaques formed by amyloid‐β (Aβ) deposition, neurofibrillary tangles caused by tau hyperphosphorylation, microglia‐evoked neuroinflammation, synaptic degeneration, and blood‐brain barrier (BBB) disruption. While the current anti‐dementia drugs are mostly single targets, Chinese medicines have great development potential considering their multi‐target anti‐dementia components.Method: Several Chinese medicine monomers, including cryptotanshinone (CTS), pterostilbene (PTE), Ginsenoside Compound K (GCK), and glabridin (Gla) were selected to test their safety and efficacy in AD cell models, and to further explore their possible molecular mechanisms and target of action. Aβ42 oligomers (AβO) were used to establish AD cell models. The cytotoxicity of AβO as well as protective effects of Chinese medicine monomers on cell models were evaluated using the MTT assay. The molecular mechanisms and pathways were tested using qRT‐PCR, ELISA, Western blot and immunofluorescence.Result: AβO induced cell injury, apoptosis, and generation of intracellular reactive oxygen species (ROS). In AβO‐induced cell models, CTS significantly reduced tau hyperphosphorylation at Ser202, Ser404, Thr181, and Thr231, and increased the levels of PSD95 and synaptophysin; PTE attenuated cell injury, apoptosis, and ROS generation; GCK diminished inflammatory cytokine production; Gla attenuated cell injury (figure1). Further study found that their mechanisms of action include PI3K/Akt/GSK3β pathway (figure2), BBB permeability and tight junction scaffold protein (figure3), as well as NF‐kB pathway via LRP1 activation (figure4), respectively.Conclusion: These results provides rational basis for the therapeutic application of Chinese medicine monomers in the treatment of AD, and support further evaluation of these multi‐target action potential in AD treatment.