Background: Coenzyme Q10 (CoQ10) is a mitochondrial cofactor with antioxidant and anti-inflammatory properties that may counteract mechanisms implicated in depression, such as oxidative stress and mitochondrial dysfunction. We evaluated the efficacy of CoQ10 supplementation on depressive symptoms and fatigue in patients with depression, whether as a primary disorder or in the context of underlying medical illness. Methods: A systematic review and meta-analysis was conducted according to PRISMA guidelines. Randomized controlled trials comparing CoQ10 with placebo or standard treatment in patients diagnosed with depression were eligible, independent of concomitant medical conditions. Outcomes included changes in depressive symptoms and fatigue. Data were pooled using random-effects models, with standardized mean differences (SMD) and 95% CIs. Heterogeneity was assessed with the I 2 statistic, and sensitivity analyses were performed using a leave-one-out approach. Results: Five RCTs with 474 participants were included. Three trials enrolled patients with depression associated with significant medical conditions—multiple sclerosis, breast cancer, and polycystic ovary syndrome—while 2 included patients with primary depressive disorders (major depression and bipolar disorder). CoQ10 supplementation significantly reduced depressive symptoms compared with control (SMD: −0.68; 95% CI: −1.02 to −0.33; P <0.01; I ² =58%), with consistent results across rating scales. Sensitivity analysis indicated that heterogeneity was largely driven by a single study. No significant benefit was observed for fatigue (SMD: −0.33; 95% CI: −1.38 to 0.72; P =0.54; I ² =89%), based on only 2 trials. Conclusions: CoQ10 supplementation may confer moderate improvement in depressive symptoms across diverse populations. However, the evidence for fatigue remains inconclusive.

Background: Donanemab, a monoclonal antibody targeting amyloid-β (Aβ) plaques, has shown the ability to reduce cerebral amyloid burden in early Alzheimer's disease (AD). However, uncertainties remain regarding its clinical relevance, particularly in relation to tau pathology, APOE ε4 genotype, and methodological limitations in existing trials. Objective: To conduct a systematic review and exploratory meta-analysis to evaluate the efficacy, safety, and tolerability of donanemab in patients with mild to moderate AD. Methods: We conducted a systematic review and exploratory meta-analysis following PRISMA guidelines. Randomized controlled trials comparing donanemab to placebo in individuals aged ≥65 years with biomarker-confirmed mild to moderate AD were included. Outcomes included cognitive measures (ADAS-Cog13, MMSE, CDR-SB, iADRS, ADCS-iADL) and adverse events (ARIA-E, ARIA-H, infusion reactions, discontinuations). Random-effects models were used to estimate pooled mean difference (MD) or risk ratio (RR) with 95% confidence intervals. Subgroup analyses were performed by baseline tau burden and APOE ε4 genotype. Results: Three trials (n = 2054) were included. Donanemab modestly reduced cognitive decline compared to placebo: ADAS-Cog13 (MD, −1.86), CDR-SB (MD, −0.36), MMSE (MD, 0.64), and iADRS (MD, 3.19), with similar effects across tau subgroups. The risk of ARIA-E was markedly increased (RR, 12.39), especially among APOE ε4 homozygotes. Infusion reactions (RR, 11.90) and discontinuations (RR, 3.22) were also more frequent. Conclusions: Donanemab demonstrated modest cognitive benefits, the clinical significance of which remains uncertain. Independent, longer-term trials with rigorous methodology and active comparators are warranted to more clearly define its therapeutic value in the treatment of AD.

Background: The no-reflow phenomenon, characterized by impaired microvascular reperfusion despite successful macrovascular recanalization, has been identified as a potential contributor to poor outcomes in acute ischemic stroke (AIS) treated with endovascular therapy (EVT). This systematic review and meta-analysis aimed to assess the prevalence and clinical impact of no-reflow phenomenon in AIS patients undergoing EVT. Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) and observational studies reporting the no-reflow phenomenon after EVT. Databases searched included PubMed, Embase, and CENTRAL (inception to February 9, 2025). Outcomes included no-reflow prevalence, functional outcomes (mRS), early neurological recovery, infarct volume, hemorrhagic complications, and 90-day mortality. Pooled risk ratios (RR) or mean differences (MD) were calculated using random-effects meta-analysis, and heterogeneity was assessed with I2. Results: Eight studies (n = 1483 patients) were included. The pooled prevalence of no-reflow was 20.5% (95% CI 6.2%–49.9%; I2 = 96.9%). Compared with controls, patients with no-reflow had reduced early neurological recovery (RR 0.76; 95% CI 0.64–0.90) and increased risk of hemorrhagic transformation (RR 1.82; 95% CI 1.18–2.79) and symptomatic intracranial hemorrhage (RR 1.88; 95% CI 1.00–3.56). Differences in functional independence (mRS 0–2) and mortality were not statistically significant. Subgroup analyses based on study design revealed divergent patterns, particularly for infarct volume, which was significantly greater in no-reflow patients in post-hoc RCTs but not in the overall analysis. Conclusion: No-reflow affects one in five EVT-treated patients and is associated with adverse neurological and hemorrhagic outcomes. Findings highlight the need for standardized definitions and prospective trials to clarify its clinical impact.