Multiple sclerosis (MS) is an immune-mediated demyelinating disorder of the central nervous system. Relevant differences between men and women are known in MS epidemiology, disease course, clinical manifestations and instrumental findings. However, differences in response to disease-modifying treatments (DMTs) have been rarely assessed. We performed a registry-based study on patients of our reference center in Palermo, Italy. Only patients with relapsing-remitting course or clinically isolated syndrome were included. Efficacy endpoints we considered were confirmed disease progression risk, first relapse risk and magnetic resonance imaging active lesion risk during treatment with each DMT. An exploratory analysis on annualized relapse risk was also performed. For safety analysis, withdrawal due to adverse events was considered. Cox multivariable survival analysis was performed to assess the impact of sex on each endpoint. one thousand eight hundred five records were retrieved. However, due to low sample size, only data regarding some drugs (dimethylfumarate, glatiramer acetate, beta interferon and partially natalizumab and S1PR modulators) were analyzed. No significant differences between the two sexes were found for efficacy endpoints. Men showed a significantly lower risk of withdrawal from glatiramer acetate due to adverse events than women (p = 0.002, hazard ratio 0.32, 95 %confidence interval 0.16-0.65); dyspnea was the most frequent cause of interruption in both sexes. Our results show limited differences in response to DMTs between men and women for the drugs we took into account. Interpretation of these findings is challenging due to limited evidence available about this topic and to sexual dysmorphism involving many aspects of the disease. Small sample size, preventing the analysis of other DMTs (especially high-efficacy ones) and disease courses, is the main limit of this study. Further evidence will be needed in the future.

Introduction: The significant impact of attention deficit/hyperactivity disorder (ADHD) on health in adult life has been widely recognized. Among the comorbidities of this disorder in later life, dementia is one of the most relevant ones. We performed a systematic review and meta-analysis to explore the impact of previous ADHD diagnosis on dementia risk. Materials and methods: We systematically searched Pubmed, Embase and Scopus for the relevant literature. Cohort and case–control studies were included in our review. Retrieved records were selected by title and abstract and then by full text reading. For quality appraisal, the Newcastle–Ottawa scale was used. A meta-analysis of hazard ratios (HRs) was performed for each type of dementia. Results: Four cohort studies and one case–control study were included, for a total of 3,703,877 and 400 participants, respectively. For all-cause dementia, the pooled HR was 2.52 (95%CI 1.51–4.22, p < 0.001), pointing out a significantly higher hazard in subjects with ADHD. For Alzheimer’s disease, vascular dementia and Lewy body dementia, no meta-analysis was performed due to the low number of available studies. Discussion and conclusions: Our results support a significant association between ADHD and risk of dementia. The results regarding specific types of dementia are more challenging to interpret and could have been influenced by sample size issues. These findings show that ADHD deserves attention in future research on cognitive disorders of the elderly; in particular, more studies are needed to reveal if a true causal relationship links ADHD and dementia.

Background/Objectives: Alzheimer’s disease (AD) is the most common cause of dementia. Among the various factors associated with the risk of AD, growing attention in recent years has focused on environmental influences, particularly air pollution. The association between air pollutants and AD remains inconclusive due to heterogeneity in available studies. Given these gaps, we performed a systematic review on the topic. Methods: We systematically searched Pubmed, Embase and Scopus. Retrieved records underwent screening by title and abstract and then in full text. We included studies quantitatively exploring the association between exposure to air pollutants and risk of AD. We performed a meta-analysis to identify a pooled estimate of the impact of each pollutant on the probability of developing AD. Results: We retrieved 1081 records and included 27 studies. We found a significant association between PM_2.5 levels and AD risk (HR 1.74, 95%CI 1.36–2.23). Our data did not support a relevant role for the other pollutants we analyzed (for PM₁₀ HR = 1.35, 95%CI: 0.86–2.11; for NO₂ HR = 1.34, 95%CI 0.96–1.86; and for O₃ HR = 1.03, 95%CI 0.68–1.57). Conclusions: PM_2.5 emerged as the pollutant most strongly and consistently associated with an increased risk of AD. This robust and statistically significant association underscores the potential neurotoxic effects of fine particulate matter. For other pollutants, a clear role was not found. These results should be interpreted with caution, due to high heterogeneity in the definition of AD in the included studies (in most cases, a clinical definition was used). More research will be needed in the future.