Introduction: Migraine is a prevalent neurological disorder causing significant disability worldwide. Despite extensive research on specific populations, comprehensive analyses of global trends are remains limited. Methods: We extracted incidence, prevalence, and disability-adjusted life years (DALYs) data for migraine from the Global Burden of Disease 2021 database. Trends were analyzed across regions, age groups, sexes, and sociodemographic index (SDI) using estimated annual percentage changes (EAPC). Predictive models (ARIMA) were used to forecast trends to 2050. Results: From 1990 to 2021, the global burden of migraine significantly increased: prevalence increased by 58.15%, from 732.56 million to 1.16 billion cases, and incidence increased by 42.06%. The DALYs also increased by 58.27%. There were differences between the sexes: female individuals had higher absolute rates of migraine incidence and prevalence, but male individuals exhibited a four- to five-fold more rapid increase than female individuals in these parameters. Adolescents (< 20 years old) have the fastest growth in prevalence and DALYs. Regionally, high SDI regions having the highest age-standardized rate (ASR) and low SDI regions having the lowest ASR in DALYs. East Asia and Latin America exhibited the most significant increases in migraine burden, whereas Southeast Asia exhibited the most pronounced decrease. Predictive analysis suggests prevalence will continue to rise until 2050, particularly among male individuals and adolescents. Conclusions: The global burden of migraine has significantly escalated from 1990 to 2021, with female individuals bearing a greater burden but male individuals showing a faster growth rate. Adolescents also face a rapidly rising prevalence. Disparities across SDI regions, countries, age groups, and sexes emphasize the need for targeted public health strategies. Focused interventions are required to mitigate the growing impact of migraines on global health, particularly among male individuals and adolescents.

Mefloquine is widely used for the treatment of malaria. However, this drug is known to induce neurological side effects including depression, anxiety, balance disorder, and sensorineural hearing loss. Yet, there is currently no treatment for these side effects. In this study, we show that the coenzyme NAD⁺, known to play a critical role in maintaining the appropriate cellular redox environment, protects cochlear axons and sensory hair cells from mefloquine-induced degeneration in cultured rat cochleae. Mefloquine alone destroyed hair cells and nerve fiber axons in rat cochlear organotypics cultures in a dose-dependent manner, while treatment with NAD⁺ protected axons and hair cells from mefloquine-induced degeneration. Furthermore, cochlear organs treated with mefloquine showed increased oxidative stress marker levels, including superoxide and protein carbonyl, and increased apoptosis marker levels, including TUNEL-positive nuclei and caspases-3. Treatment with NAD⁺ reduced the levels of these oxidative stress and apoptosis markers. Taken together, our findings suggest that that mefloquine disrupts the cellular redox environment and induces oxidative stress in cochlear hair cells and nerve fibers leading to caspases-3-mediated apoptosis of these structures. Exogenous NAD⁺ suppresses mefloquine-induced oxidative stress and prevents the degeneration of cochlear axons and sensory hair cells caused by mefloquine treatment.

Obstructive sleep apnea (OSA) is independently associated with dyslipidemia. Previous studies have demonstrated that sleep fragmentation can impair lipid metabolism. The present study aimed to identify whether sleep fragmentation is independently associated with dyslipidemia, in a large-scale, clinic-based consecutive OSA sample. This cross-sectional study was conducted among 2,686 patients who underwent polysomnography (PSG) for suspicion of OSA from January 2008 to January 2013 at the sleep laboratory. Multivariate regression analyses were performed to evaluate the independent associations between the microarousal index (MAI) and lipid profiles adjusting for potential confounders, including metabolic syndrome components and nocturnal intermittent hypoxia. The adjusted odds ratios (ORs) for various types of dyslipidemia according to MAI quartiles, as determined by logistic regression were also evaluated. MAI was found positively associated with low-density lipoprotein cholesterol (LDL-c) but not with total cholesterol (TC), triglyceride (TG) or high-density lipoprotein cholesterol (HDL-c). Furthermore, the adjusted ORs (95% confidence interval) for hyper-LDL cholesterolemia increased across MAI quartiles, as follows: 1 (reference), 1.3 (1.1–1.7), 1.6 (1.2–2.0) and 1.6 (1.2–2.1) (p = 0.001, linear trend). Sleep fragmentation in OSA is independently associated with hyper-LDL cholesterolemia, which may predispose patients with OSA to a higher risk of cardiovascular disease.

Background Dyslipidaemia is an intermediary exacerbation factor for various diseases but the impact of obstructive sleep apnoea (OSA) on dyslipidaemia remains unclear. Methods A total of 3582 subjects with suspected OSA consecutively admitted to our hospital sleep centre were screened and 2983 (2422 with OSA) were included in the Shanghai Sleep Health Study. OSA severity was quantified using the apnoea–hypopnea index (AHI), the oxygen desaturation index and the arousal index. Biochemical indicators and anthropometric data were also collected. The relationship between OSA severity and the risk of dyslipidaemia was evaluated via ordinal logistic regression, restricted cubic spline (RCS) analysis and multivariate linear regressions. Results The RCS mapped a nonlinear dose–effect relationship between the risk of dyslipidaemia and OSA severity, and yielded knots of the AHI (9.4, 28.2, 54.4 and 80.2). After integrating the clinical definition and RCS-selected knots, all subjects were regrouped into four AHI severity stages. Following segmented multivariate linear modelling of each stage, distinguishable sets of OSA risk factors were quantified: low-density lipoprotein cholesterol (LDL-C), apolipoprotein E and high-density lipoprotein cholesterol (HDL-C); body mass index and/or waist to hip ratio; and HDL-C, LDL-C and triglycerides were specifically associated with stage I, stages II and III, and stages II–IV with different OSA indices. Conclusions Our study revealed the multistage and non-monotonic relationships between OSA and dyslipidaemia and quantified the relationships between OSA severity indexes and distinct risk factors for specific OSA severity stages. Our study suggests that a new interpretive and predictive strategy for dynamic assessment of the risk progression over the clinical course of OSA should be adopted.