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Meta-analyses incorporating the Systolic Blood Pressure Intervention Trial (SPRINT) have shown a reduced incidence of dementia with blood pressure lowering. However, mechanistic explanations for this effect are lacking, apart from slowed progression of cerebral white matter lesions (WML). Here we examine possible biomarkers of angiogenesis related to small vessel brain disease including bFGF, FLT1, PLGF, TIE-2, VEGF, VEGF-C, and VEGF-D. The biomarkers were assayed in plasma at baseline and during follow-up (median follow-up = 3.8 years) in a subgroup of participants 60 to 89 years old from SPRINT (N=517). We modeled changes in each biomarker using robust linear mixed models accounting for treatment group, time since randomization, and kidney function. Participants were 69.8 ± 7.1 (standard deviation) years of age, 42.1% female, with a mean systolic blood pressure (SBP) of 138.2 ± 17.0 mm Hg. At baseline, none of the biomarkers were associated with WML lesion volume or total brain volumes adjusting for age (all p>0.05), while FLT1, PLGF, and TIE-2 were negatively associated with frontal gray matter cerebral blood flow (partial correlations of -0.11, -0.10, and -0.12 respectively, all p

ALDH2*2 is a loss of function mutation common in East Asian populations associated with facial flushing on exposure to alcohol and increased risk of certain cancers. Conversely, absence of the ALDH2*2 mutation is associated with increased risk of hypertension and cerebral microbleeds, and two recent studies report a higher frequency of ALDH2*2 alleles in nonagenarians compared to population control samples. We used survival analysis to investigate the association between ALDH2*2 and risk of cognitive impairment and death after controlling for midlife alcohol consumption and other covariates. Participants are 621 Japanese-American men (72 to 92) enrolled in the Honolulu Asia Aging Study (HAAS) and assessed for cognitive impairment for up to 20 years. Impairment was defined as crossing below a threshold score of 74 on the Cognitive Assessment Screening Instrument (CASI). Age at death was determined by Hawaii state death certificate. Ounces of ethyl alcohol consumed per month was assessed by structured interview (number, frequency, and type of beverage) conducted 25 years prior to baseline cognitive assessment. Persons heterozygous for the ALDH2*2 variant have reduced risk of cognitive impairment and reduced risk of death, compared to homozygote non-carriers. Covarying by alcohol exposure had no effect on observed associations. This study replicates previous findings associating ALDH2*2 with longevity, and provides evidence the protective effect extends to cognition. This poster details the statistical analysis carried out to obtain these results.

Introduction: We aim to investigate the longitudinal associations between social participation and the risk of developing mild cognitive impairment (MCI|) and dementia over 5 years of follow-up among cognitively normal older adults. Methods: A total of 2802 participants had complete follow-up data from Age-Gene/Environment-Susceptibility-Reykjavik-Study. Social participation was assessed by a questionnaire asking the frequency of contact with children, relatives, friends and neighbors. MCI and dementia were diagnosed according to international guidelines and by a team composed of a geriatrician, neurologist, neuropsychologist, and neuroradiologist. Logistic regression analysis was used to assess the associations. Results: At baseline 8% (n=225) reported no social participation. Among cognitively normal participants at baseline, 5.6% (n=243) developed mild cognitive impairment and 2.4% (n= 103) developed dementia during a mean follow-up time of 5.2 years. After full adjustment with covariates including age, gender, education, marital status, vitamin D levels, depression and APOE ε4, those with no social participation at baseline were significantly more likely to develop MCI at follow-up (OR=1.953, P=0.001). However, social participation at baseline was not associated with higher dementia diagnosis at follow-up (OR= 1.490, P=0.194). Conclusions: Community-dwelling old adults who are socially inactive are more likely to develop MCI than those who are socially active. Social participation might independently indicate impending changes in cognitive function among older adults.