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While transgender and gender non-binary (trans/nb) individuals are disproportionately affected by HIV, pre-exposure prophylaxis (PrEP) uptake remains low in this underserved population. We conducted four focus groups with 37 trans/nb individuals in San Diego and Los Angeles to assess barriers and facilitators of PrEP usage. Transcripts were coded for qualitative themes. Although overall PrEP awareness was high, participants reported limited knowledge and misinformation about PrEP. Barriers to PrEP use included: structural access (e.g., discrimination from health care providers, lack of trans-inclusive services, financial barriers), mental health struggles limiting ability to access PrEP, and concerns about potential side effects, drug-drug interactions with hormone therapy, and lack of other STI protection. Facilitators of PrEP usage included: increased PrEP availability, prior experience taking daily medications, and motivation to have active and healthy lives without fear of contracting HIV. Addressing both structural and psychosocial/behavioral factors in trans-affirming health care environments is crucial to designing inclusive, effective PrEP interventions.

INTRODUCTION: The geroscience hypothesis proposes systemic biological aging is a root cause of cognitive decline. METHODS: We analyzed Framingham Heart Study Offspring Cohort data (n = 2296; 46% male; baseline age M = 62, SD = 9, range = 25–101 y). We measured cognitive decline across two decades of neuropsychological‐testing follow‐up. We measured pace of aging using the DunedinPACE epigenetic clock. Analysis tested if participants with faster DunedinPACE values experienced more rapid cognitive decline compared with those with slower DunedinPACE values. RESULTS: Participants with faster DunedinPACE had poorer cognitive functioning at baseline and experienced more rapid cognitive decline over follow‐up. Results were robust to confounders and consistent across population strata. Findings were similar for the PhenoAge and GrimAge epigenetic clocks. DISCUSSION: Faster pace of aging is a risk factor for preclinical cognitive decline. Metrics of biological aging may inform risk stratification in clinical trials and prognosis in patient care. Highlights: Faster DunedinPACE is associated with preclinical cognitive aging. Higher baseline cognition was protective of DunedinPACE‐associated cognitive decline. The DunedinPACE association with cognitive decline explained a fourth of dementia risk. [ABSTRACT FROM AUTHOR]

Background: Biomarkers that predict the heterogenous nature and late onset of cognitive decline are needed to evaluate geroscience interventions designed to delay or prevent the progression of Alzheimer's Disease and related dementias (ADRD). The DunedinPACE epigenetic clock is designed to measure pace of biological aging, and is therefore a promising candidate biomarker. Here we (1) investigate if DunedinPACE is associated with cognitive aging, and (2) the extent to which these associations are independent of education. Method: We analyzed data from the Framingham Heart Study Offspring Cohort. Our analysis sample included participants with neuropsychological testing data and blood DNA methylation data collected within 14 months of their baseline cognitive assessment (n = 2,296 non‐Hispanic White adults, 46% male; M age = 61.6 ± 9.0 [25‐101y]). A series of growth curve models tested the interactive effects of DundeinPACE and education upon baseline and longitudinal changes in global unadjusted T scores. All models included covariates to adjust for cellular composition of blood samples, smoking status, sex, age at baseline (specified as a quadratic term), and date of blood draw. Result: A faster DunedinPACE was associated with worse global cognition, and steeper decline in cognition over time (Bs = ‐.37 ‐ ‐.45; ps<.001). After adjusting for education, DunedinPACE remained robustly associated with global cognition and steeper decline in cognition over time (Bs = ‐.33 ‐ ‐38; ps<.01). In effect modification analyses, higher education buffered the effect of faster DunedinPACE upon global cognition at baseline (B = ‐.21; p<.01), but did not significantly modify the effect of DunedinPACE upon cognitive decline over time (p =.95). Conclusion: The presented findings support prior work that highlight the role of systemic biological aging in cognitive decline, and further validates the utility of the epigenetic clock, DunedinPACE, as a potential biomarker for decline in cognitive aging. Further validation of DunedinPACE and its clinical utility as a biomarker for geroscience interventions targeting ADRD is warranted. Greater years of education appears to mitigate some of the deleterious effect of biological aging upon cognition. Future studies should critically examine these relationships among nationally representative samples and diverse samples disproportionately impacted by ADRD. [ABSTRACT FROM AUTHOR]

People living with HIV (PLWH) report higher rates of cannabis use than the general population, a trend likely to continue in light of recent policy changes and the reported therapeutic benefits of cannabis for PLWH. Therefore, it is important to better understand cannabis-associated effects on neurocognition, especially as PLWH are at heightened risk for neurocognitive impairment. This study aimed to elucidate the effects of a past cannabis use disorder on current neurocognition in a diverse sample of PLWH. This cross-sectional study included 138 PLWH (age M(SD) = 47.28(8.06); education M(SD) = 12.64(2.73); 73% Male; 71% Latinx) who underwent neuropsychological, DSM-diagnostic, and urine toxicology evaluations. One-way ANCOVAs were conducted to examine effects of a past cannabis use disorder (CUD+) on tests of attention/working memory, processing speed, executive functioning, verbal fluency, learning, memory, and motor ability. Compared to the past CUD- group, the past CUD+ group performed significantly better on tests of processing speed, visual learning and memory, and motor ability (p's <.05). Findings suggest PLWH with past cannabis use have similar or better neurocognition across domains compared to PLWH without past use. [ABSTRACT FROM AUTHOR]

Introduction: The geroscience hypothesis proposes systemic biological aging is a root cause of cognitive decline., Methods: We analyzed Framingham Heart Study Offspring Cohort data ( n  = 2296; 46% male; baseline age M  = 62, SD = 9, range = 25-101 y). We measured cognitive decline across two decades of neuropsychological-testing follow-up. We measured pace of aging using the DunedinPACE epigenetic clock. Analysis tested if participants with faster DunedinPACE values experienced more rapid cognitive decline compared with those with slower DunedinPACE values., Results: Participants with faster DunedinPACE had poorer cognitive functioning at baseline and experienced more rapid cognitive decline over follow-up. Results were robust to confounders and consistent across population strata. Findings were similar for the PhenoAge and GrimAge epigenetic clocks., Discussion: Faster pace of aging is a risk factor for preclinical cognitive decline. Metrics of biological aging may inform risk stratification in clinical trials and prognosis in patient care., Highlights: Faster DunedinPACE is associated with preclinical cognitive aging.Higher baseline cognition was protective of DunedinPACE-associated cognitive decline.The DunedinPACE association with cognitive decline explained a fourth of dementia risk., Competing Interests: A.C., T.E.M., K.S., and D.W.B. are inventors of the Duke University and University of Otago Invention DunedinPACE, which is licensed to TruDiagnostic. There are no other conflicts of interest., (© 2024 The Author(s). Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)

Objective: This study describes trajectories of cognitive aging among American Indian/Alaskan Native (AI/AN) adults with and without HIV and the role of immunosenescence longitudinally., Method: We characterized trajectories of cognitive aging in a sample of 333 AI/AN and 309 non-Hispanic White (NHW) adults who were followed longitudinally for up to 20 years by the HIV Neurobehavioral Research Program (HNRP) across six U.S. research sites. We used growth curve modeling with autoregressive Lag-1 structures and heterogeneous residual variances to assess the role of ethnoracial identity and HIV grouping upon decline in trajectories of cognitive aging., Results: HIV- AI/AN adults demonstrated earlier and steeper decline in normative trajectories of cognitive aging on tasks of processing speed, timed tasks of attention/working memory, executive function, and psychomotor speed in comparison to HIV- NHW adults. Accentuated trajectories of cognitive aging were evident in both HIV+ and HIV+ immunosuppressed groups in comparison to HIV- peers and were primarily driven by the role of immunosenescence., Conclusions: AI/AN disparities in trajectories of cognitive aging are evident and are likely explained by the interplay of biopsychosociocultural factors, including immunosenescence. (PsycInfo Database Record (c) 2024 APA, all rights reserved).