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Background African Americans are among the most vulnerable demographic groups to both sleep deficiencies and Alzheimer’s disease (AD)3. ABCA7‐80 (rs115550680) known as adenosine triphosphate (ATP)‐binding cassette member 7, plays a role in the transport of amyloid precursor protein, clearance of cellular Aβ, and lipid metabolism: three processes associated with late‐onset AD2. Slow oscillations, which characterize non‐REM sleep, are implicated in waste clearance and memory consolidation in the brain1. The present study investigated the putative association between ABCA7‐80 risk on non‐REM slow wave oscillations among cognitively unimpaired older African Americans. Method Participants were drawn from the ongoing longitudinal study, Pathways to Healthy Aging in African Americans conducted at Rutgers University–Newark. 75 participants, ages 60‐87 years old completed a saliva test for genotyping and underwent at‐home sleep monitoring over two nights using the DREEM 3 Headband. MANCOVA statistical analysis was performed on the sample data. Result Individuals with the ABCA7‐80 high‐risk allele, had significantly lower frontal slow oscillation relative power than individuals with the non‐risk allele (F= 2.175, η 2= 0.137, p= 0.084). Conclusion This preliminary data shows that individuals who have the ABCA7‐80 high‐risk genotype may have lower slow oscillation relative power. This holds importance for AD in African Americans as there is evidence that ABCA7‐80 is more relevant for cognitively unimpaired older African Americans.

Background Older African Americans bear a disproportionate burden of both sleep problems and cognitive dysfunction. Alarmingly, poorer sleep health may put an individual at higher risk of cognitive dysfunction. However, the relationship between sleep and cognition in older African Americans continues to be understudied. This study aimed to examine the relationship between subjective sleep health characteristics and cognitive function among older African Americans. Method 62 older African American participants (mean age = 72.19; SD = 6.651; mean education = 14.28; SD = 6.651; 51 female; 11 male) from the Pathways to Healthy Aging in African Americans study completed a demographic questionnaire as well as cognitive assessments of attention, episodic memory, executive function, language, and global cognition. The following sleep health characteristics were derived from the Pittsburgh Sleep Quality Index: Subjective sleep quality; sleep latency; sleep duration; sleep disturbances; use of sleeping medications; daytime dysfunction; and global index score. Hierarchical linear regression analyses were employed to investigate the relationship between sleep health characteristics and cognitive function while controlling for age, sex, education, waist‐to‐hip ratio, and depressive symptomology. Result The relationship between subjective sleep quality and episodic memory (B = ‐1.715; p < 0.001); sleep disturbances and global cognition (B = ‐1.581; p = 0.020); sleep latency and global cognition (B = ‐1.033; p = .011); and sleep efficiency and attention (B = 0.249; p = 0.038) were significant before and after controlling for covariates. Overall, poorer sleep health across multiple characteristics was associated with worse cognitive function. Conclusion Self‐reported sleep disturbances and longer sleep latency appear to be tapping into poorer global cognition, whereas poorer subjective sleep quality and sleep efficiency are tapping into worse episodic memory and attention, respectively. These findings highlight the importance of assessing self‐reported sleep health in populations at higher risk for both sleep disorders and cognitive dysfunction.

Background Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by amyloid plaques and neurofibrillary tangles which cause neurodegeneration and cognitive decline1. APOE‐ε4 is identified as the first common genetic risk factor with high penetrance in the early onset of AD3. ABCA7 (rs115550680) (ABCA7‐80) is associated with the development of late‐onset AD among African Americans2. The medial temporal lobe (MTL) is the first region that displays atrophy and neurofibrillary tangle involvement during AD4. However, the comparative influence of APOE‐ε4 and ABCA7‐80 on neural functions among African Americans is not yet known. The present study investigated the effect of APOE‐ε4 and ABCA7‐80 high‐risk alleles on the MTL dynamic network flexibility among cognitively unimpaired older African Americans. Method 175 older, cognitively unimpaired African Americans drawn from the ongoing longitudinal study, Pathways to Healthy Aging in African Americans completed saliva collection for genotyping and underwent an MRI scan in a Siemens 3T Prisma scanner. AFNI and ANTs were used for dynamic functional MRI processing and analysis for MTL dynamic network flexibility. Gender, age, and education were used as covariates for analysis. Result The analysis revealed trend‐level differences in MTL Dynamic network flexibility between high‐risk and non‐risk allele carriers for ABCA7‐80 (F = 3.531, η² = 0.025, p = 0.062) and for APOE‐ε4 allele (F = 2.421, η² = 0.017, p = 0.122). Individuals with the ABCA7‐80 high‐risk allele exhibited significantly lower MTL dynamic network flexibility compared to those with the APOE‐ε4 allele (F = 4.577, η² = 0.067, p = 0.036). Conclusion ABCA7‐80 high‐risk allele may better capture the dynamic neural dysfunction in the MTL network rather than APOE‐ε4 among cognitively unimpaired older African Americans.

Background Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by amyloid plaques and neurofibrillary tangles which cause neurodegeneration and cognitive decline1. APOE‐ε4 is identified as the first common genetic risk factor with high penetrance in the early onset of AD3. ABCA7 (rs115550680) (ABCA7‐80) is associated with the development of late‐onset AD among African Americans2. The medial temporal lobe (MTL) is the first region that displays atrophy and neurofibrillary tangle involvement during AD4. However, the comparative influence of APOE‐ε4 and ABCA7‐80 on neural functions among African Americans is not yet known. The present study investigated the effect of APOE‐ε4 and ABCA7‐80 high‐risk alleles on the MTL dynamic network flexibility among cognitively unimpaired older African Americans. Method 175 older, cognitively unimpaired African Americans drawn from the ongoing longitudinal study, Pathways to Healthy Aging in African Americans completed saliva collection for genotyping and underwent an MRI scan in a Siemens 3T Prisma scanner. AFNI and ANTs were used for dynamic functional MRI processing and analysis for MTL dynamic network flexibility. Gender, age, and education were used as covariates for analysis. Result The analysis revealed trend‐level differences in MTL Dynamic network flexibility between high‐risk and non‐risk allele carriers for ABCA7‐80 (F = 3.531, η² = 0.025, p = 0.062) and for APOE‐ε4 allele (F = 2.421, η² = 0.017, p = 0.122). Individuals with the ABCA7‐80 high‐risk allele exhibited significantly lower MTL dynamic network flexibility compared to those with the APOE‐ε4 allele (F = 4.577, η² = 0.067, p = 0.036). Conclusion ABCA7‐80 high‐risk allele may better capture the dynamic neural dysfunction in the MTL network rather than APOE‐ε4 among cognitively unimpaired older African Americans.

Background Advancing age is typically associated with a decline in memory capacity and increased risk of Alzheimer’s disease (AD)1. However, there is a subgroup of the older adult population defined as SuperAgers that presents excellent memory performance reflecting resilience to the typical and pathological pathways of aging 2. Atrophy in hippocampal subregions, key areas for memory formation, are early anatomical markers of preclinical AD3. Plasma p‐tau levels, particularly p‐tau 231, also show sensitivity to preclinical AD neuropathology.4 This study aimed to investigate structural neuroimaging and plasma biomarker differences between the SuperAger phenotype and typical agers among African Americans. Method Participants were drawn from the ongoing longitudinal study, Pathways to Healthy Aging in African Americans conducted at Rutgers University–Newark. 100 participants (matched for SuperAger and typical ager status) completed a neuroimaging visit and a blood draw for plasma biomarkers. AFNI and ANTs were used for the segmentation of the medial temporal lobe and hippocampal regions of interest. Furthermore, plasma aliquots were sent for p‐tau 231 processing via Quanterix Simoa™. Result SuperAgers had lower levels of p‐tau 231, (t(19) = 2.85, p = 0.010, d = 20.38) than typical agers suggesting reduced AD neuropathology burden. African American SuperAgers also had greater DG/CA3 volumes, (t(19) = ‐2.756, p = 0.013, d = 46.42) than typical agers. Conclusion SuperAgers demonstrated larger hippocampal subregions implicated in memory formation and lower plasma p‐tau levels suggesting potential neuroprotective mechanisms in this unique population. SuperAgers may represent a valuable model for understanding cognitive resilience and for developing novel therapeutic strategies to mitigate age‐related cognitive decline and AD.

Background Biomarkers, such as blood p‐tau181, p‐tau217, and p‐tau231, have been created and verified to mirror the pathophysiology of tau and amyloid‐β (Aβ) in the brain 2. Sleep spindles are known to contribute to memory consolidation and generalization and may therefore be a promising biomarker in preclinical Alzheimer’s Disease (AD) 3,4,5. The present study investigated the relationship between sleep spindles and p‐tau levels in cognitively healthy older African Americans. Method Participants were drawn from the ongoing longitudinal study, Pathways to Healthy Aging in African Americans conducted at Rutgers University–Newark. 75 participants, ages 60‐87 years old (completed a blood draw and underwent at‐home sleep monitoring over two nights using the DREEM 3 Headband. Plasma was extracted from blood samples to assess p‐tau 231 levels using Single molecule array technology, measured by in‐house Simoa methods at the University of Gothenburg. Based on the sample median thresholds, a subset of participants were characterized as having higher p‐tau231 levels (> 8.9447 pg/mL). Result Individuals with high levels of p‐tau 231 (> 8.9447 pg/mL) had significantly lower frontal sleep spindle relative power than individuals with lower p‐tau 231 levels (< 8.9447 pg/mL) (F= 1.110, η 2= 0.175, p= 0.378). Conclusion Sleep spindle relative power may serve as a potential marker for p‐tau231 levels among cognitively unimpaired older African Americans in preclinical AD.

Introduction We determined risk profiles of strata-specific cognitive-normal (NL) older-adults with obstructive sleep apnea (OSA) characterized by their Aβ, P-Tau & T-tau (ATN) burden, on prospective AD stage-transition Methods Longitudinal study utilizing data from 167 community-dwelling NL older-adults participating in NYU studies on memory, sleep and aging. Subjects had baseline CSF AD-biomarker data and at least two follow-up clinical and neuropsychological data. OSA was defined using AHI4%. Using the NIA-AA Research Framework, data-driven, clinically relevant thresholds for CSF-Aβ42 (≤375pg/ml), P-tau (≥53.7pg/ml) and T-tau (≥367 pg/ml) indicated ATN status respectively. Twenty-four participants with suspected non-AD pathologic change defined as A-T+ were excluded leaving 143 for the analysis. Main outcome was AD stage-transition (i.e., change from Global Deterioration Scale (GDS) 1 or 2 [NL] at baseline to ≥3 [≥ MCI] during follow-up). Logistic mixed-effects models with random intercept and slope were used to assess associations between ATN characterized OSA subjects, and longitudinal AD stage transition, controlling for age-at-baseline, sex, APOE4-status, years-of-education, and their interactions with time. Results Of the 143 participants, 91 (63.8%) were women. The mean (SD) age was 69.6 (7.3) years and follow-up time was 4.73 (3.45) years. Sixteen (11.2%) were OSA+/A+/TN-, and 21 (14.7%) were OSA-/A+/TN-. Ninety-two (64.3%) had normal AD biomarkers (OSA+/A-/T- [n=45] and OSA-/A-/T- [N=47]). To generate strata-specific risks, subjects were combined into groups: (i) OSA subjects with AD pathologic change OSA+/A+/TN [n=25] consisting of OSA+/A+/TN+ [n=9] plus OSA+/A+/TN- [n=16] (ii) non-OSA subjects with AD pathologic change OSA-/A+/TN [n=26]) consisting of OSA-/A+/TN+ [n=5] and OSA-/A+/TN- [n=21] Fourteen subjects (9.8%) transitioned from NL to MCI (i.e., OSA+/A+/TN [6/25], OSA-/A+/TN [3/26], OSA+/A-/TN- [4/45] and OSA-/A-/TN- [3/47]). OSA+/A+/TN subjects were at higher risk of AD stage-transition relative to OSA-/A-/TN- (β = 1.31, 95%CI, 1.02, 1.62); OSA+/A-/TN- (β = 0.89, 95%CI, 0.42, 1.37); and OSA-/A+/TN subjects, (β = 0.71, 95%CI, 0.38, 1.04); P < .01 for all. OSA+/A-/T- vs. OSA-/A-/T- participants did not show differences in cognitive change over time (β = 0.22, 95%CI, -0.15, 0.39, P =.17). Conclusion Among ATN characterized NL older-adults with OSA, those with evidence of AD pathologic change have the greatest risk of developing AD. Support (if any) AASMBTS#231-BS-20, NIAK23AG068534A, AARG-D- 21-848397, BFFA2022033S

Introduction We determined whether slow wave sleep is associated with plasma levels of Aβ40, Aβ42, Aβ42/Aβ40, Tau, tau/Aβ42 and NfL and whether this relationship differed between Blacks/African-Americans and non-Hispanic Whites. Methods This was a cross-sectional analysis of baseline data from 171 community-dwelling cognitively normal older-adults, participating in ongoing NYU studies on memory, sleep and aging. Non-rapid eye movement sleep (NREM) slow wave sleep (SWS) duration was calculated from 2 nights of in-lab NPSGs. Plasma Aβ40, Aβ42, Tau and NfL were determined using single molecule array (SIMOA). Associations of NREM SWS duration and plasma AD biomarker levels were assessed using adjusted generalized linear models and Pearson correlation analysis after data normalization. Analyses were adjusted for age, sex, BMI, race, and education. Results Of the 171 subjects (128 non-Hispanic Whites and 43 Blacks/African-Americans), 112 (65.5%) were females, and mean (SD) age was 68.6 (6.6) years, BMI was 27.6 (6.1) kg/m**2, and education was 16.9 (2.1). There were no racial differences in age, sex, BMI, NREM SWS and AHI4%. Compared to non-Hispanic Whites, Blacks/African-Americans had significantly lower years of education (14.2 vs. 17.2, p <.01), plasma Aβ40 (248.3 vs. 262.5 pg/ml) and NfL levels (11.4 vs. 15.2 pg/ml) p<.05 for both. There were no significant racial differences in levels of plasma Aβ42, Aβ42/Aβ40, Tau, Tau/Aβ40 and Tau/Aβ42 (p>.05 for all). NREM SWS duration was not associated with plasma Aβ42, Aβ40 or tau in the overall sample (p>.05 for all). However, in non-Hispanic Whites, NREM SWS negatively correlated with plasma Aβ42 (r=-0.28, p<=0.05), plasma Aβ40 (r=-0.087, p=0.72), though not significant, and plasma Tau (r=-0.153, p=0.27), though not significant. In Black/African-Americans, NREM SWS positively correlated with plasma Aβ42 (r=0.48, p=0.05), plasma Aβ40 levels (r=0.32, p=0.04), and plasma Tau levels (r=0.52, p=0.04). NREM SWS was not associated with plasma tau/Aβ42, plasma tau/Aβ40 or plasma NfL in the overall sample and across racial subgroups. Conclusion Race-specific divergent associations between NREM SWS and plasma Aβ42, Aβ40 & Tau may suggest differences in SDOH factors and mechanisms that could influence sleep and AD-risk in older-adults. Support (if any) AASMBTS#231-BS-20, NIAK23AG068534A, AARG-D- 21-848397, BFFA2022033S