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Amyotrophic lateral sclerosis (ALS) is a fast-progressing neurodegenerative disease with a median survival time from diagnosis of 1.5–3 years. The cause of ALS is unknown, but inflammation may play a role. Fiber has been shown to lower inflammatory markers, and a high fiber intake was associated with a lower risk of ALS in a case-control study; however, prospective studies are lacking. We explored the relation between dietary intake of fiber and the risk of ALS in 5 large prospective cohort studies comprising over 1,050,000 US citizens who contributed 1,133 ALS cases during a mean of 15 years of follow-up (1980–2008). Cox proportional hazards models were used within each cohort, and cohort-specific estimates were subsequently pooled using a random-effects model. We found that intakes of total fiber, cereal fiber, vegetable fiber, and fruit fiber were not associated with ALS risk when comparing the highest quintile of intake with the lowest (for total fiber, pooled multivariable relative risk (RR) = 0.99, 95% confidence interval (CI): 0.80, 1.24; for cereal fiber, RR = 1.13, 95% CI: 0.94, 1.37; for vegetable fiber, RR = 0.97, 95% CI: 0.77, 1.23; and for fruit fiber, RR = 1.05, 95% CI: 0.86, 1.29). These findings do not support the hypothesis that fiber intake is a major determinant of ALS risk. [ABSTRACT FROM PUBLISHER]

A recent meta-analysis of 7 genome-wide association studies on early balding (alopecia) revealed single nucleotide polymorphism variants in the region of the amyotrophic lateral sclerosis (ALS) gene TAR DNA-binding protein 43 (TARDBP/TDP-43). We therefore explored the association of early-onset alopecia and ALS in the Health Professionals Follow-up Study, a large cohort of 51,529 US men. In 1992, the participants (then aged 46–81 years) were asked to report their hair line pattern at age 45 years. During the follow-up period (1992–2008), 42 men were diagnosed with ALS. Of those, 13 had reported no alopecia, 18 had reported moderate alopecia, and 11 had reported extensive alopecia at age 45 years. Those who reported extensive alopecia had an almost 3-fold increased risk of ALS compared with those who reported no alopecia (relative risk = 2.74, 95% confidence interval: 1.23, 6.13). Furthermore, we observed a linear trend of increased risk of ALS with increasing level of balding at age 45 years (Ptrend = 0.02). In conclusion, men with early-onset alopecia seem to have a higher risk of ALS. The mechanisms underlying this association deserve further investigation. [ABSTRACT FROM PUBLISHER]

Background: Little is known about how multiple sclerosis (MS) presents in Hispanic/Latinx (HL) people with MS (pwMS)., Objective: Compare age at onset (AAO) and onset severity between HL versus non-Hispanic White (NHW) pwMS., Methods: A cross-sectional study leveraged the MS PATHS registry spanning seven US tertiary care institutions. HL was subcategorized as HL White (HLW) and HL Other (HLO; all other races). Multivariable models examined relationships between ethnoracial variables and AAO and self-reported presenting disease course. Models were repeated restricting to those born ⩾1970., Results: The study population included 8231 pwMS, including 540 HL (200 HLW, 340 HLO). The sex distribution did not differ across ethnoracial subgroups. From the statistical models (1) HLO pwMS had an earlier AAO and a higher prevalence of initial progressive disease course than NHW pwMS; (2) among all HL pwMS, irrespective of race, AAO did not differ by sex or between relapsing and progressive MS at onset. In younger HLO adults (born ⩾1970), those with progressive MS at onset had an earlier AAO than those with relapsing MS; and (3) in HL pwMS there was no sex-bias in presenting disease course., Discussion: Distinct differences in the presentation of MS in HL compared with NHW individuals were observed., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Objective: Comorbid anxiety occurs often in MS and is associated with disability progression. Polygenic scores offer a possible means of anxiety risk prediction but often have not been validated outside the original discovery population. We aimed to investigate the association between the Generalized Anxiety Disorder 2-item scale polygenic score with anxiety in MS., Methods: Using a case-control design, participants from Canadian, UK Biobank, and United States cohorts were grouped into cases (MS/comorbid anxiety) or controls (MS/no anxiety, anxiety/no immune disease or healthy). We used multiple anxiety measures: current symptoms, lifetime interview-diagnosed, and lifetime self-report physician-diagnosed. The polygenic score was computed for current anxiety symptoms using summary statistics from a previous genome-wide association study and was tested using regression., Results: A total of 71,343 individuals of European genetic ancestry were used: Canada (n = 334; 212 MS), UK Biobank (n = 70,431; 1,390 MS), and the USA (n = 578 MS). Meta-analyses identified that in MS, each 1-SD increase in the polygenic score was associated with ~50% increased odds of comorbid moderate anxious symptoms compared to those with less than moderate anxious symptoms (OR: 1.47, 95% CI: 1.09-1.99). We found a similar direction of effects in the other measures. MS had a similar anxiety genetic burden compared to people with anxiety as the index disease., Interpretation: Higher genetic burden for anxiety was associated with significantly increased odds of moderate anxious symptoms in MS of European genetic ancestry which did not differ from those with anxiety and no comorbid immune disease. This study suggests a genetic basis for anxiety in MS., (© 2024 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.)

Background: Hypertension adversely impacts the multiple sclerosis (MS) disease course and is more common among Black Americans. Disparities in care due to structural racism may lead to suboptimal hypertension detection and control in Black American MS patients., Objectives: To determine if uncontrolled hypertension is more common in Black or White Americans with MS and whether race impacts the likelihood of receiving anti-hypertensive treatment., Methods: A retrospective cohort study was conducted using longitudinal data from American participants in the Multiple Sclerosis Partners Advancing Technology and Health Solutions (MS PATHS) multi-institutional registry. Data was collected from 7 sites in the United States between May 2015 and November 2020. Patients with uncontrolled hypertension, defined as ≥2 blood pressure measurements ≥140/90 mmHg, were identified in the dataset. Racial differences in uncontrolled hypertension and odds of anti-hypertensive treatment were evaluated using logistic regression. Predictors of anti-hypertensive treatment in those with uncontrolled hypertension were determined by race., Results: The analysis included 10,673 MS patients, of whom 1,442 (13.5%) were Black Americans. Despite a lower mean age (45.7 vs. 49.2 years), Black Americans had a 31% increased odds of uncontrolled hypertension compared to White Americans. After adjustment for relevant covariates, mean systolic blood pressure was 1.84 mmHg (95% confidence interval=1.07-2.61) higher in Black Americans than White Americans, and mean diastolic blood pressure was 1.28 mmHg (95% confidence interval=0.74-1.82) higher. Black Americans were also more likely to be on anti-hypertensive therapy (OR=1.68, 95% confidence interval=1.30-2.18) and were exposed to an adjusted average of 0.61 (95% confidence interval=0.45-0.78) more anti-hypertensive treatments than White Americans (p<0.001). Age, comorbid diabetes mellitus, and comorbid hyperlipidemia were positively associated with use of anti-hypertensive treatments in all patients with uncontrolled hypertension., Conclusion: Black American MS patients have significantly increased odds of uncontrolled hypertension, but also higher odds of receiving anti-hypertensive treatment., (Copyright © 2022. Published by Elsevier B.V.)

Background: Integrase strand transfer inhibitors (INSTIs) are first-line regimens for HIV treatment. We aimed to examine their impact on cognitive performance and depressive symptoms in women with HIV (WWH)., Setting: Women's Interagency HIV Study, a multisite, prospective, cohort study., Methods: WWH who started or switched to INSTI-based antiretroviral therapy (ART) and completed neuropsychological testing and the Center for Epidemiological Studies-Depression (CES-D) scale before and after INSTI start/switch were included in the analyses. Primary outcomes were demographically corrected cognitive domain T-scores. Linear mixed-effects models adjusted for relevant covariates were used to examine effects of start/switch of any INSTI and individual INSTI drugs on cognition and CES-D scores., Results: Six hundred thirty-nine WWH, median age 49 (interquartile range 12) years, 66% Black non-Hispanic, had neuropsychological and CES-D scale data before and after INSTI start/switch. Although 14% started INSTI-based ART, the remainder switched to INSTI-based ART from another regimen. Overall, any INSTI use was associated with poorer learning post-INSTI. Specifically, use of dolutegravir and elvitegravir, but not raltegravir, was associated with poorer learning. In analyses restricted to INSTI switch, any INSTI use, and dolutegravir use, was associated with poorer learning. Among those switching from a PI-based regimen, INSTIs overall and dolutegravir remained associated with poorer learning; switching from a nonnucleoside reverse transcriptase inhibitor to dolutegravir was also associated with poorer learning. INSTI start/switch was not related to depressive symptom changes., Conclusions: INSTI use was associated with poorer learning among WWH. These changes were mainly observed in elvitegravir and dolutegravir users, indicating that the impact of INSTI on cognition in WWH may not be a class effect., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Background: People with multiple sclerosis (MS) may be at higher risk for complications from the 2019 coronavirus (COVID-19) pandemic due to use of immunomodulatory disease modifying therapies (DMTs) and greater need for medical services., Objectives: To evaluate risk factors for COVID-19 susceptibility and describe the pandemic's impact on healthcare delivery., Methods: Surveys sent to MS patients at Cleveland Clinic, Johns Hopkins, and Vall d'Hebron-Centre d'Esclerosi Múltiple de Catalunya in April and May 2020 collected information about comorbidities, DMTs, exposures, COVID-19 testing/outcomes, health behaviors, and disruptions to MS care., Results: There were 3028/10,816 responders. Suspected or confirmed COVID-19 cases were more likely to have a known COVID-19 contact (odds ratio (OR): 4.38; 95% confidence interval (CI): 1.04, 18.54). In multivariable-adjusted models, people who were younger, had to work on site, had a lower education level, and resided in socioeconomically disadvantaged areas were less likely to follow social distancing guidelines. 4.4% reported changes to therapy plans, primarily delays in infusions, and 15.5% a disruption to rehabilitative services., Conclusion: Younger people with lower socioeconomic status required to work on site may be at higher exposure risk and are potential targets for educational intervention and work restrictions to limit exposure. Providers should be mindful of potential infusion delays and MS care disruption.

Background: Exposure to air pollution has been implicated in a number of adverse health outcomes and the effect of particulate matter (PM) on the brain is beginning to be recognized. Yet, no prospective study has examined the association between PM and risk of Parkinson Disease. Thus, our goal was assess if exposure to particulate matter air pollution is related to risk of Parkinson's disease (PD) in the Nurses' Health Study (NHS), a large prospective cohort of women., Methods: Cumulative average exposure to different size fractions of PM up to 2 years before the onset of PD, was estimated using a spatio-temporal model by linking each individual's places of residence throughout the study with location-specific air pollution levels. We prospectively followed 115,767 women in the NHS, identified 508 incident PD cases and used multivariable Cox proportional hazards models to estimate the risk of PD associated with each size fraction of PM independently., Results: In models adjusted for age in months, smoking, region, population density, caffeine and ibuprofen intake, we observed no statistically significant associations between exposure to air pollution and PD risk. The relative risk (RR) comparing the top quartile to the bottom quartile of PM exposure was 0.99 (95% Confidence Intervals (CI): 0.84,1.16) for PM10 (≤10 microns in diameter), 1.08 (95% CI: 0.81, 1.45) for PM2.5 (≤2.5 microns in diameter), and 0.92 (95% CI: 0.71, 1.19) for PM(10-2.5) (2.5 to 10 microns in diameter)., Conclusions: In this study, we found no evidence that exposure to air pollution is a risk factor for PD.