Aim To investigate the prevalence of metabolic syndrome and cardiovascular disease (CVD) risk factors and the association between common metabolic markers and Gross Motor Function Classification System (GMFCS) levels in ambulatory adults with cerebral palsy (CP). Method Metabolic markers and GMFCS levels were evaluated in a cross‐sectional study of 70 ambulatory adults with CP (34 males, 36 females; mean age 24y 5mo [SD 5y 4mo], range 18y 6mo–48y 8mo) to determine the prevalence of metabolic syndrome and CVD risk factors, and were compared to age‐matched, population norms from the National Health and Nutrition Examination Survey (NHANES) registry. The Framingham Heart Study (FHS) CVD risk estimation was also used to evaluate an individual's risk for CVD. Results Metabolic syndrome was identified in 17.1% of the cohort, higher than the 10% in the NHANES registry. The FHS CVD 30‐year lipid and body mass index (BMI)‐based risk factor results showed that 20% to 40% of the cohort was at greater risk of developing CVD (BMI‐based: 39.7% ‘full’ CVD risk factor; lipid‐based: 26.5% ‘full’ CVD risk factor) as compared to the FHS normative population data. There was a positive correlation between GMFCS level, waist circumference (r=0.28, p=0.02), and waist‐to‐hip ratio (r=0.28, p=0.02). Interpretation Adults with CP are at higher risk of CVD and metabolic syndrome compared to the general population, which is probably because of impaired mobility. What this paper adds Gross Motor Function Classification System levels can predict cardiovascular disease (CVD) risk factors in adults with cerebral palsy (CP). Anthropometric measures are significant in predicting CVD risk factors in adults with CP. Early CVD screening and ongoing risk factor monitoring are important in adults with CP.

Clinically, individuals with cerebral palsy (CP) experience symptoms of accelerated biological aging. Accumulative deficits in both molecular underpinnings and functions in young adults with CP can lead to premature aging, such as heart disease and mild cognitive impairment (MCI). MCI is an intermediate stage between healthy aging and dementia that normally develops at old age. Owing to their intriguingly parallel yet “inverted” disease trajectories, CP might share similar pathology and phenotypes with MCI, conferring increased risk for developing dementia at a much younger age. Thus, we examined this hypothesis by evaluating these two distinct populations (MCI= 55, CP = 72). A total of nine measures (e.g., blood biomarkers, neurocognition, Framingham Heart Study Score (FHSS) were compared between the groups. Compared to MCI, upon controlling for covariates, delta FHSS, brain-derived neurotrophic factor (BDNF) levels, and systolic blood pressure were significantly lower in CP. Intriguingly, high-sensitivity CRP, several metabolic outcomes, and neurocognitive function were similar between the two groups. This study supports a shared biological underpinning and key phenotypes between CP and MCI. Thus, we proposed a double-hit model for the development of premature aging outcomes in CP through shared biomarkers. Future longitudinal follow-up studies are warranted to examine accelerated biological aging.

PURPOSE: To understand the relationship of walking speed to self-reported pain, fatigue, and physical function in adults with CP. METHODS: Design: Cross-sectional study. Setting: Accredited clinical motion analysis laboratory in a regional children's hospital. Participants: 72 ambulatory patients 18 years of age, diagnosed with CP, who previously had 1 prior instrumented gait analysis at our facility. Main Outcome Measures: PROMIS-57 pain interference/intensity, physical function, and fatigue measures and walking speed. RESULTS: Physical function was significantly lower than able-bodied normal values by 1-2 standard deviations (40.3 ± 8.5). Pain interference (51.4 ± 9.0) and fatigue (50.2 ± 9.2) were not significantly different when compared to able-bodied normal values. Only physical function was statistically correlated with walking speed (p < 0.001), while pain interference (p = 0.39), pain intensity (p = 0.36), and fatigue (p = 0.75) were not. Pain interference, pain intensity, and fatigue were not statistically significant factors in the multiple regression of walking speed. Fatigue could significantly predict physical function, pain interference, and pain scores (p = 0.032, p < 0.001, p < 0.01, respectively), however, fatigue did not directly predict walking speed (p = 0.747). CONCLUSIONS: Self-reported physical function correlates with objectively measured walking speed in young adults with CP while patient-reported pain and fatigue did not, contrary to what would be predicted by the literature.

Background: Previous meta-analyses examining the continuum of Alzheimer’s disease (AD) concluded significantly decreased peripheral brain-derived neurotrophic factor (BDNF) in AD. However, across different meta-analyses, there remain inconsistent findings on peripheral BDNF levels in individuals with mild cognitive impairment (MCI). This issue has been attributed to the highly heterogenous clinical and laboratory factors. Thus, BDNF’s level, discriminative accuracy for identifying all-cause MCI and its subtypes, and its associations with other biomarkers and neurocognitive domains, remain largely unknown. Methods: To address this heterogeneity, we compared a healthy control cohort (n=56, 45 female) to an MCI cohort (n=40, 28 female), to determine whether plasma BDNF, hs-CRP, and DHEA-S can differentiate healthy from MCI individuals, including two MCI subtypes (amnestic [aMCI] and non-amnestic [non-aMCI]). The associations between BDNF with other biomarkers and neurocognitive tests were examined. Adults with cerebral palsy were included as sensitivity analyses. Results: Compared to healthy controls, BDNF was significantly higher in all-cause MCI, aMCI, and non-aMCI. Furthermore, BDNF had good (AUC=0.84, 95% CI=0.74 to 0.95, p<0.001) and excellent discriminative accuracies (AUC=0.92, 95% CI=0.84 to 1.00, p<0.001) for all-cause MCI and non-amnestic MCI, respectively. BDNF was significantly and positively associated with plasma hs-CRP (β=0.26, 95% CI=0.02 to 0.50, p=0.038), despite attenuated association upon controlling for BMI (β=0.15, 95% CI=-0.08 to 0.38, p=0.186). Multiple inverse associations between BDNF and detailed neurocognitive tests were also detected. Conclusions: These findings suggest BDNF is increased as a compensatory mechanism in preclinical dementia, supporting the neurotrophic and partially the inflammatory hypotheses of cognitive impairment.