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BACKGROUND: Traffic-related air pollution is emerging as a risk factor for Alzheimer's disease (AD) and impaired brain development. Individual differences in vulnerability to air pollution may involve the ∊4 allele of Apolipoprotein E (APOE) gene, the primary genetic risk factor for AD. OBJECTIVE: We analyzed whether the association between traffic air pollution and neurodevelopmental outcomes is modified by APOE ∊4 status in children. METHODS: Data on parent-reported behavior problems (total difficulties scores, Strengths and Difficulties Questionnaire), teacher-reported attentiondeficit hyperactivity disorder (ADHD) symptom scores, cognitive performance trajectories (computerized tests of inattentiveness and working memory repeated 2-4 times during January 2012-March 2013), and APOE genotypes were obtained for 1,667 children age 7-11 y attending 39 schools in or near Barcelona. Basal ganglia volume (putamen, caudate, and globus pallidum) was measured in 163 of the children by MRI (October 2012-April 2014.) Average annual outdoor polycyclic aromatic hydrocarbons (PAHs), elemental carbon (EC), and nitrogen dioxide (NO2 concentrations were estimated based on measurements at each school (two 1-wk campaigns conducted 6 months apart in 2012). RESULTS: APOE ∊4 allele carriers had significantly higher behavior problem scores than noncarriers, and adverse associations with PAHs and NO2 were stronger or limited to ∊4 carriers for behavior problem scores (P-interaction 0.03 and 0.04), caudate volume (P-interaction 0.04 and 0.03), and inattentiveness trajectories (P-interaction 0.15 and 0.08, respectively). Patterns of associations with the same outcomes were similar for EC. CONCLUSION: PAHs, EC, and NO2 were associated with higher behavior problem scores, smaller reductions in inattentiveness over time, and smaller caudate volume in APOE ∊4 allele carriers in our study population, and corresponding associations were weak or absent among ∊4 noncarriers. These findings support a potential role of APOE in biological mechanisms that may contribute to associations between air pollution and neurobehavioral outcomes in children. [ABSTRACT FROM AUTHOR]

Background: Cerebral sulci openings have been consistently observed as larger in Alzheimer's disease (AD) patients than in cognitively normal elderly. However, it remains unknown whether large openings may have predictive value of cognitive trajectories. We aimed to determine whether sulci openings might be predictors of changes in cognition over a 3‐year period in elderly people at risk to develop AD (at‐AD‐risk). Method: Participants were recruited in memory and research centers in France between 2008 and 2011 in the framework of the MRI‐Multidomain Alzheimer Preventive Trial (MRI‐MAPT) ancillary study. They were non‐demented community‐dwelling women and men aged ≥ 70 years, and presented memory complaints and frailty criteria. In 20 sulci distributed throughout the brain, openings were extracted from Magnetic Resonance Imaging (MRI) T1‐weighted images obtained at baseline in 433 participants, using the Morphologist pipeline of BrainVISA [http://brainvisa.info, version 4.5.1]. Cognition was evaluated at baseline, 6, 12, 24, and 36 months of follow‐up with a composite Z score combining four cognitive tests (free and total recall of the Free and Cued Selective Reminding test, ten Mini‐Mental State Examination (MMSE) orientation items, Digit Symbol Substitution Test, and Category Naming Test). Linear mixed regression models explored the composite score variation over time according to the baseline openings magnitude. Result: At baseline, participants were on average 74.8 (4.0) years old. The mean MMSE was 28.1 (1.5) and the mean composite cognitive score was 0.11 (0.62). Sulci openings were categorized into tertiles (T1, T2, T3) for the statistical analyses. The participants showing the largest openings (T3) in the left anterior inferior temporal sulcus presented a greater decline in the composite cognitive score over the 3‐year period of follow‐up (β=‐0.07, 95%CI [‐0.12; ‐0.02]) than the participants with lower openings values. Conclusion: Large openings of sulci within the lateral temporal area of the brain might be predictors of cognitive decline within 3 years in at‐AD risk individuals. These results may have strong applications in clinical setting and for preventive strategies. [ABSTRACT FROM AUTHOR]

Background: Anxiety is common in patients with cognitive impairment and dementia. However, whether anxiety is a risk factor for dementia is still not known. We aimed to examine the association between trait anxiety at baseline and the 10-year risk of incident dementia to determine to which extent depressive symptoms influence this relationship in the general population. Methods: Data came from 5,234 community-dwelling participants from the Three-City prospective cohort study, aged 65 years at baseline and followed over 10 years. At baseline, anxiety trait was assessed using the Spielberger State-Trait Anxiety Inventory (STAI), and depressive symptoms using Center for Epidemiologic Studies-Depression Scale (CESD). Use of anxiolytic drugs was also considered. Diagnoses of dementia were made at baseline and every 2 years. To examine the relationship between anxiety exposures and risk of incident dementia, Cox proportional hazard regression models were performed. Results: Taking anxiolytic drugs or having high trait anxiety (STAI score ≥ 44) increased the risk of dementia assessed over 10 years of follow-up [Hazard Ratio (HR) = 1.39, 95%CI: 1.08-1.80, p = 0.01 and HR = 1.26, 95%CI: 1.01-1.57, p = 0.04, respectively], independently of a large panel of socio-demographic variables, health behaviors, cardio-metabolic disorders, and additional age-related disorders such as cardiovascular diseases, activity limitations, and cognitive deficit. However, the associations were substantially attenuated after further adjustment for depressive symptoms. Conclusion: Our findings suggest that depressive symptoms shape the association between anxiety trait and dementia. Further research is needed to replicate our findings and extrapolate our results to anxiety disorders.