Disclosure and self-efficacy among HIV-positive men who have sex with men: A comparison between older and younger adults

Men who have sex with men (MSM) continue to be disproportionately affected by HIV in the US. HIV among older adults also continues to be an important public health problem. Age is associated with disclosure of HIV serostatus and self-efficacy for condom use. However, studies examining self-efficacy and disclosure among older MSM (age 50 and older) living with HIV are lacking. The aim of this study was to assess the associations between being 50 and older, and disclosure behaviors, intentions and attitudes, and self-efficacy for condom use, disclosure, and negotiation for safer sex practices among HIV-positive MSM. Data were gathered from 340 participants at the baseline assessment of a longitudinal disclosure intervention study. Linear regression was used to determine the association between being older (age 50 and older) and disclosure behaviors, intentions and attitudes, and self-efficacy for condom use, disclosure, and negotiation for safer sex practices. After adjusting for time since diagnosis and number of sexual partners, MSM aged 50 and older scored lower in disclosure behavior (beta = -7.49; 95% CI: -14.8, -0.18) and in self-efficacy for negotiation of safer sex practices (beta = -0.80; 95% CI: -1.57, -0.04) compared to MSM 18-34 years. Intervention and prevention programs should endeavor to improve disclosure and self-efficacy for negotiating safer sex practices among older HIV-positive MSM. More health care providers should initiate sexual health discussions, especially among older HIV-positive MSM populations, which may help to improve their disclosure behavior and self-efficacy for negotiating safer sex practices

Interaction of obstructive sleep apnea severity and amyloid burden on novel plasma biomarkers of tau and neurofilament light protein in community‐dwelling cognitively normal older‐adults

Background Recent evidence suggest that plasma Tau and neurofilament light (NfL) have high potential as markers of neurodegeneration in Alzheimer disease (AD). Obstructive sleep apnea (OSA) severity increases AD risk and is associated with well‐validated markers of AD pathology in cognitively normal older‐adults. We determined the independent and combined effects of OSA severity and amyloid burden on plasma levels of Tau, and NfL, in community‐dwelling cognitively normal older‐adults. Method Cross‐sectional analysis of baseline data from 70 community‐dwelling cognitively normal older‐adults, selected from ongoing NYU prospective longitudinal studies on memory, sleep and aging. CSF‐Aβ42 (measured using ELISA) quantified amyloid burden. OSA severity was defined using AHI4%. Levels of plasma Tau and NfL were determined using single molecule array (SIMOA) technology ultra‐sensitive assays. Associations of OSA severity and plasma Tau and NfL were assessed using Pearson correlation analysis. The interactive associations of OSA severity and CSF‐Aβ42 levels on plasma Tau and NfL was assessed using generalized linear models. Analyses were adjusted for age, sex, BMI, education and APOE4. Result Of the 70 participants, 42 (60%) were women. Mean (SD) age was 68.7 (7.1) years. Mean (SD) AHI was 11.4/hr. (13.7) {29 (40%) had AHI 30}. Independent of CSF‐Aβ42, OSA severity was not associated with plasma Tau (r=.11, p‐value=.38), or plasma NfL (r=.05, p‐value=.67). The interactive associations of OSA severity and CSF‐Aβ42 levels on plasma Tau (β =0.042; 95% CI, 0.013 to 0.070) and NfL (β = 0.055; 95% CI, 0.022 to 0.089) were significant, P < .05 for all. The analysis was not powered for generating dichotomized strata specific (i.e. OSA+/Aβ+, OSA+/Aβ‐, OSA‐/Aβ+ and OSA‐/Aβ‐) estimates. Conclusion In this sample of cognitively normal older‐adults, OSA severity was not associated with plasma levels of Tau and NfL. However, β estimates of the interactive associations of OSA severity and CSF‐Aβ42 levels suggest that their combined effect is associated with higher plasma levels of Tau or NfL. Larger cohorts are necessary to delineate mechanisms and examine for OSA/Aβ strata‐specific estimates

Effect of APOE genotype on the Association between Sleep Disturbance and Cognition across Racial/Ethnic groups

Background APOE alleles are associated with cognitive‐decline and Alzheimer’s disease in Whites. We examined the effect of APOE‐genotype on the association between sleep disturbance (SD) and cognition across racial/ethnic groups. Method We conducted a cross‐sectional analysis of baseline data on 10,254 (i.e., 7900 non‐Hispanic Whites, 1428 Black/African‐Americans, 627 Hispanics and 299 Asians) cognitive‐normal subjects from the National Alzheimer’s Coordinating Center Uniform Dataset. We characterized SD using an item on the Neuropsychiatric Inventory‐Questionnaire. Generalized linear models examined SD‐group differences (i.e., SD vs. no SD) on psychometric tests performance between‐and‐within racial categories. The interactive associations of APOE genotype, SD, and race on psychometric tests performance was also examined. All models included age, sex, education, hypertension, and diabetes. Result Overall, the mean (sd) age was 71.1 (10.3) years and education was 15.7 (3.0) years. Prevalence of SD was 10% (Whites), 6.1% (Blacks), 18.2% (Hispanics), and 7.4% (Asians). SD subjects were at increased risk for worse psychometric scores in: executive, and language domains (p < 0.02 for all) among Whites; language domain (p = 0.001) among Blacks; memory, executive, and language domains (p ≤0.05 for all) among Hispanics; and visuospatial memory domain (p ≤0.001) among Asians. The interactive associations of APOE genotype, SD, and race on psychometric tests performance were significant (p ≤0.001 for all). Within racial groups, only Hispanic SD subjects with 1 or 2 APOE ε4 alleles were at increased risk for worse psychometric scores in memory, executive function, visuospatial, attention, processing speed and language domains (p ≤0.001 for all). Compared to Whites and Asians, Hispanic and Black SD subjects were at increased risk for worse psychometric scores across all domains (p ≤0.001 for all), regardless of APOE‐ε4 status. Conclusion In this sample of cognitive‐normal older‐adults, SD subjects were at increased risk for worse psychometric scores in specific cognitive domains that varied by race/ethnicity. Hispanic and Black SD subjects were at increased risk for worse psychometric scores regardless of APOE‐ε4 status. APOE‐ε4 effect on SD‐cognition association worsened psychometric scores and occurred only within Hispanics. These findings suggest that APOE‐ε4 interacts with sleep to effect varying cognitive domain outcomes within‐and‐between racial/ethnic groups

Interactive associations of nocturnal sleep disturbance and vascular risk with prospective cognitive decline in clinically normal elderly individuals: Findings from the National Alzheimer's Coordinating Center Uniform Data Set

Background We determined whether Nocturnal Sleep Disturbance (NSD) and vascular risk act together to promote prospective cognitive‐decline in clinically normal older adults; and, evaluated the unique influence of their combined risk on prospective cognitive decline beyond that of commonly used Alzheimer’s disease (AD) biomarkers. Method Longitudinal study utilizing data from the National Alzheimer's Coordinating Center (NACC) Uniform Data set (UDS). Participants (N=361) were cognitively normal at baseline and had baseline medical data to quantify vascular risk, using an adaptation of the Framingham Heart Study general cardiovascular disease (aFHS‐CVD) risk‐score and CSF‐Aβ, CSF P‐tau, CSF T‐tau and MRI‐imaging data with at least one UDS follow‐up visit. The Neuropsychiatric Inventory Questionnaire characterized NSD and incident mild cognitive impairment (MCI) diagnosis during UDS follow‐up characterized prospective cognitive decline. Logistic mixed‐effects models with random intercept and slope, controlling for age, sex, education, APOE‐ε4 and their interactions with time examined associations between the NSD/ FHS‐CVD risk score and longitudinal cognitive‐decline. Result Of the 361 participants, 223 (62%) were women and 35 (9.7%) had NSD. The proportion of males versus females with sleep problems was 10.9% vs. 9.3% respectively. For participants with NSD and no NSD, the mean (SD) age was 71 (7.3) and 70 (5.7) years and average follow‐up time was 5.2 (2.6) and 4.9 (2.7) years, respectively. Both NSD (OR: 1.42, P < .003) and higher aFHS‐CVD risk score (OR; 1.63, P < .001) were significantly associated with increased/faster likelihood to develop incident MCI. The interaction of NSD and the aFHS‐CVD risk‐score with time was significant (P < .001) suggesting an increase in the likelihood of conversion to MCI increased over time. Stratifying aFHS‐CVD risk score into tertiles, NSD participants in the highest (OR: 2.82, P < .003) and middle tertile (OR: 2.38, P < .001) were significantly more likely to develop incident MCI, compared with participants without NSD in the lowest aFHS‐CVD risk score tertile, suggesting a synergistic effect. This effect remained robustly associated with incident MCI even after adjustment for AD biomarkers. Conclusion In elderly cognitive‐normal individuals, NSD and vascular risk may be alternate and non‐invasive measures of assessing risk of prospective cognitive‐decline in preclinical AD

0645 Associations of Objective Sleep Parameters and Gray Matter Microstructure in community dwelling cognitive normal older adults

Abstract Introduction Disturbed sleep measures differentially alter white-matter microstructure. We examined whether obstructive sleep apnea (OSA)-severity, sleep fragmentation and duration measures were associated with gray-matter diffusion tensor-imaging metrics (DTI) (i.e., fractional anisotropy [FA], mean diffusivities [MD] and kurtoses [MK]) in community-dwelling cognitive-normal older-adults. Methods Gray-matter DTI metrics from MRI including mean FA, MD and MK measures of the hippocampus, thalamus, medial prefrontal-cortex (mPC) and Alzheimer’s Disease (AD) vulnerable regions (temporal [inferior, middle, and superior], parietal [inferior and superior], entorhinal cortex, and precuneus) were determined from 85 subjects. OSA-severity measures included AHI3a and AHI4%. Other sleep measures included sleep efficiency (SE), non-rapid eye movement (NREM) slow wave sleep (SWS) duration, percent time spent in SWS (%SWS), slow wave activity (SWA), total sleep time (TST), and wake after sleep onset (WASO). To analyze the data, first, we utilized factor analysis using varimax rotation to account for the DTI metrics as multivariate outcomes. Using factor loadings, we anticipated a two or three-factor model was sufficient to explain the variance of the DTI metrics. Second, we investigated predictive associations between the sleep parameters and the loaded DTI factors, and explored age, sex, BMI, education and APOE4 as covariates underlying any differences. Results Of the 85 participants, 60 (70.6%) were women, 67 (78.8%) were non-Hispanic Whites. Mean (SD) age, BMI and education was 66.7 (5.3) years, 27.9 (6.1) kg/m2 and 16.8 (2.4) years respectively. We selected the two primary loadings’ factor model based on AIC criteria. FA metrics of the investigated brain regions except thalamus, loaded on one factor, conceptualized as manifest indicators for FA. MD and MK metrics of all the investigated brain regions loaded on the second factor, conceptualized as manifest indicators for MD/MK. SWS, %SWS, TST were predictors of FA (P ≤0.01 for all). AHI3a, AHI4%, and SWA were predictors of MD/MK (P ≤0.05 for all). Additionally, sex, age, APOE4 and education were predictors of FA (P ≤0.01 for all). Conclusion In this limited sample of cognitively-normal older-adults, sleep duration measures predicted gray-matter FA, OSA-severity measures predicted gray matter MD and MK. Demographic, genetic and SES factors explained the differences in these relationships. Support (If Any) AASM 231-BS-20, AARGD-21-8488397, NIH/NIA/NHLBI (K23AG068534, L30-AG064670, CIRAD P30AG059303 Pilot, NYU ADRC P30AG066512 Developmental Grant, R25HL105444, SRG, R01AG12101, R01AG022374, R01AG13616, RF1AG057570, R01HL118624, R01AG056031