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Learn more: PMC Disclaimer | PMC Copyright Notice Alzheimers Dement (Amst) . 2026 Apr 11;18(2):e70324. doi: 10.1002/dad2.70324 Search in PMC Search in PubMed View in NLM Catalog Add to search Subjective memory concerns and AD/ADRD plasma biomarker associations in HABS‐HD Kelsey R Thomas Kelsey R Thomas 1 University of California San Diego, La Jolla, California, USA 2 VA San Diego Healthcare System, San Diego, California, USA Find articles by Kelsey R Thomas 1, 2, ✉ , Caitlin M Terao Caitlin M Terao 3 San Diego Joint Doctoral Program in Clinical Psychology, San Diego State University/University of California, San Diego, California, USA Find articles by Caitlin M Terao 3 , Alexandra J Weigand Alexandra J Weigand 3 San Diego Joint Doctoral Program in Clinical Psychology, San Diego State University/University of California, San Diego, California, USA 4 Memory and Aging Center, University of California San Francisco, San Francisco, California, USA Find articles by Alexandra J Weigand 3, 4 , Melissa Petersen Melissa Petersen 5 University of North Texas Health Science Center, Fort Worth, Texas, USA Find articles by Melissa Petersen 5 , Sid O'Bryant Sid O'Bryant 5 University of North Texas Health Science Center, Fort Worth, Texas, USA Find articles by Sid O'Bryant 5 , Alexandra L Clark Alexandra L Clark 6 The University of Texas at Austin, Austin, Texas, USA Find articles by Alexandra L Clark 6 ; HABS‐HD Study Team Author information Article notes Copyright and License information 1 University of California San Diego, La Jolla, California, USA 2 VA San Diego Healthcare System, San Diego, California, USA 3 San Diego Joint Doctoral Program in Clinical Psychology, San Diego State University/University of California, San Diego, California, USA 4 Memory and Aging Center, University of California San Francisco, San Francisco, California, USA 5 University of North Texas Health Science Center, Fort Worth, Texas, USA 6 The University of Texas at Austin, Austin, Texas, USA * Correspondence , Kelsey R. Thomas, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. Email: [email protected] ✉ Corresponding author. Revised 2026 Mar 9; Received 2025 Jul 11; Accepted 2026 Mar 11; Collection date 2026 Apr-Jun. © 2026 The Author(s). Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals LLC on behalf of Alzheimer's Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. PMC Copyright notice PMCID: PMC13069461 PMID: 41971641 Abstract INTRODUCTION We examined relationships among subjective memory concerns (SMC), plasma biomarkers, and objective memory within racially/ethnically diverse older adults. METHODS Participants included 1618 cognitively unimpaired older adults (681 Hispanic/Latino [H/L], 164 non‐Hispanic Black [NHB], 773 non‐Hispanic White [NHW]) from the Health and Aging Brain Study–Health Disparities. Associations among SMC, plasma biomarkers (phosphorylated tau 181 [p‐tau181], amyloid beta 42/40 [Aβ42/40], neurofilament light chain [NfL], total tau [t‐tau]), and objective memory were examined. RESULTS Higher SMC was associated with higher plasma p‐tau181 and NfL levels in NHW participants only. Higher depressive symptoms were associated with higher plasma p‐tau181 in NHB participants only. Higher SMC related to lower objective memory for H/L and NHW participants. Plasma biomarkers had unique patterns of association with memory tests by racial/ethnic group. DISCUSSION Different patterns of subjective memory, objective memory, and plasma biomarker associations within racial/ethnic groups suggests variability in the utility of SMC for early detection of Alzheimer's disease–related changes. Keywords: AD/ADRD, memory, plasma biomarkers, subjective cognitive decline, subjective memory concern Highlights Subjective memory concerns related to plasma biomarkers in White older adults only. Depressive symptoms related to plasma phosphorylated tau181 in Black participants only. Subjective memory related to objective memory in Hispanic/Latino and White participants. Plasma biomarkers differentially related to memory scores by racial/ethnic group in HABS‐HD. 1. BACKGROUND With increased accessibility of more reliable biomarkers, Alzheimer's disease (AD) and AD‐related dementias (ADRD) research has moved toward earlier detection to promote intervention prior to widespread neurodegeneration. 1 Within the National Institute on Aging–Alzheimer's Association (NIA‐AA) 2018 AD Research Framework 2 and in the revised 2024 AA Workgroup criteria, 3 clinical stage 2 represents individuals who may experience subtle cognitive decline, captured by either subjective report or evidence of very mild objective decline, but who do not yet meet criteria for mild cognitive impairment (MCI). While the AA Workgroup focuses on a biomarker‐only definition of AD, they have also stated that biomarker testing should not be conducted in individuals without clinical symptoms. 3 The International Working Group (IWG) uses a different approach for defining AD and states that cognitive symptoms are a critical part of the AD definition itself, which is a clinical–pathologic diagnosis. 4 , 5 Thus, the identification of clinically meaningful subtle cognitive decline would support the goals of both the AA Workgroup as well as the IWG recommendations that emphasize the importance of early detection of clinical changes. Subjective cognitive decline (SCD) has been discussed as a viable indicator of subtle cognitive changes due to AD/ADRD, 6 and multiple studies indicate that subjective memory concerns (SMC) 7 are associated with AD/ADRD outcomes such as amyloid, tau, neurodegeneration, and cognition. 8 , 9 , 10 However, multiple factors have been shown to impact the associations between SMC and AD‐related outcomes. For example, associations between SCD and progression to dementia, neuroimaging outcomes, and cognition have been shown to vary by study setting such that SCD is more useful in clinic samples than community‐based samples. 11 , 12 , 13 Additionally, depressive symptoms or longstanding personality traits may attenuate the prognostic utility of SMC on future declines. 10 , 13 , 14 The literature is also mixed in regard to whether SMC are predictive of objective cognition and AD‐related outcomes across racial/ethnic groups. 15 , 16 , 17 Some studies have shown no difference in SCD relationships by race/ethnicity. 18 However, others have shown the relationship between SCD and objective cognition may be weaker in Hispanic/Latino and Black older adults relative to White older adults, 15 , 16 , 19 and more closely tied to depressive symptomology rather than objective cognition in racially minoritized older adults. 16 , 19 , 20 Conversely, another study showed that greater SCD was associated with higher risk of progression to dementia, and this effect was stronger for Black and Latinx older adults than White participants. 21 Within Hispanic/Latino older adults specifically, higher SCD and SMC have been linked to poorer global and domain‐specific cognition, and lower entorhinal and hippocampal volumes. 20 , 22 , 23 Different patterns of endorsing SCD may be partially responsible for some of these mixed findings. One study has shown a differential pattern such that non‐Hispanic White older adults were more likely to endorse SCD in the absence of objective cognitive impairment, while in contrast, Black and Hispanic older adults were less likely to endorse SCD in the context of objective cognitive impairment. 17 Presently, relatively little is known about the associations between SMC and ADRD biomarkers within racially/ethnically diverse older adults. One study found that race moderated the relationship between amyloid positron emission tomography (PET) and subjective cognitive concerns, such that cognitive concerns related to amyloid burden in non‐Hispanic White and Asian older adults but not in Black or Hispanic/Latino older adults. 16 Notably, racially/ethnically minoritized groups in this study were relatively small and additional research in larger, representative samples are needed. Furthermore, associations between SMC and plasma ADRD biomarkers remain unexplored and are needed to clarify the utility of SMC as an index of early AD pathologic change. Therefore, the current study examined the associations of SMC with plasma ADRD biomarkers as well as objective memory performance within Hispanic/Latino (H/L), non‐Hispanic Black (NHB), and non‐Hispanic White (NHW) older adults from the Health and Aging Brain Study–Health Disparities (HABS‐HD). RESEARCH IN CONTEXT Systematic review : The authors reviewed the literature using traditional approaches (e.g., Google Scholar, PubMed). There is a vast literature on the role of subjective memory concerns (SMC) and Alzheimer's disease (AD)‐related outcomes in cognitively unimpaired individuals, though the literature is more limited within Hispanic/Latino and Black/African American older adults, and findings within these racial/ethnic groups are mixed. Interpretation : Our findings suggest that there may be different patterns of associations between subjective memory, objective memory, and plasma AD and AD‐related dementias biomarkers in cognitively unimpaired Hispanic/Latino, non‐Hispanic Black, and non‐Hispanic White older adults that may indicate unique mechanisms underlying these subtle changes. Future directions : Future work should continue to explore more sensitive markers of cerebrovascular and inflammation changes that may be more closely linked to SMC in Hispanic/Latino and non‐Hispanic Black older adults, as well as the role of psychosocial factors in the utility of subjective memory concerns for early risk detection. 2. METHODS 2.1. Data availability HABS‐HD is a single‐site community‐based research study that seeks to understand ADRD risk in racially/ethnically diverse older adults that reside in the Dallas and Fort Worth, Texas metropolitan area. 24 HABS‐HD data are publicly available and consist of cognitive, behavioral, clinical lab, blood plasma, brain magnetic resonance imaging (MRI) and PET scans assessments. Written informed consent was obtained for all study participants and HABS‐HD was approved by the University of North Texas Health Science Center Institutional Review Board. Data from HABS‐HD release 3 were used to maximize the number of available participants in which the same plasma biomarker assay was used for phosphorylated tau 181 (p‐tau181). 2.2. Participants Detailed inclusion and exclusion criteria for HAB‐HD have been detailed elsewhere. 24 The current study included baseline data from 1618 cognitively unimpaired (CU) participants aged 50 to 90 years old, including 681 H/L, 164 NHB, and 773 NHW older adults. CU status was based on consensus diagnoses by HABS‐HD clinicians such that participants generally had a Clinical Dementia Rating (CDR) Sum of Boxes score of 0 and neuropsychological test scores within normal limits (i.e., demographically adjusted cognitive scores better than 1.5 standard deviation [SD] below the mean). 24 Participants with a subjective cognitive concern who otherwise meet criteria for CU were considered CU. 25 HABS‐HD participants classified as having MCI or dementia based on a consensus diagnosis were excluded from the current study. All included participants completed neuropsychological testing, the Subjective Memory Complaints Questionnaire (SMCQ), and had blood‐based AD/ADRD biomarkers. There is a relatively lower number of NHB participants because recruitment of this cohort began later and some NHB participants had a different plasma p‐tau181 assay at their baseline visit; note only those with the same assay as the H/L and NHW participants were included for current analyses. 2.3. SMCQ SMC were captured using the SMCQ, a 14‐item measure of self‐reported memory concerns. Each binary (yes/no) item was summed, with scores ranging from 0 (i.e., no self‐reported memory concerns) to 14 (i.e., high self‐reported memory concerns). This measure has been shown to have adequate internal consistency (α > 0.8) across multiple cohorts 26 , 27 and has excellent fit as a single factor in HABS‐HD, with no‐to‐minimal differential item functioning across age, sex, education, and ethnicity/language in the sample. 26 2.4. Objective memory performance Objective memory performance was measured with a composite score that was derived using immediate and delayed recall trials of Logical Memory stories from the Wechsler Memory Scale (WMS)‐III 28 and total immediate recall of trials 1 through 5 and delayed recall scores from the Spanish‐English Verbal Learning Test (SEVLT). 29 The composite score was created by first z scoring the four raw scores across the whole sample. Next, the mean of the z scores was calculated to create the overall composite score. Follow‐up analyses also examined each of the four memory tests separately, because some of the scores may be more sensitive to early changes in this CU sample. 2.5. Plasma biomarkers Plasma p‐tau181, amyloid beta 42/40 (Aβ42/40) ratio, neurofilament light chain (NfL), and total tau (t‐tau) were collected as part of the HABS‐HD protocol and were assayed using single molecule array (Simoa) technology (Quanterix) and run on the HD‐X Automated Immunoassay Analyzer. 24 , 30 These methods have been described elsewhere. 25 Briefly, plasma samples were processed in accordance with reported guidelines for sample preparation and storage. Higher p‐tau181, NfL, and t‐tau and lower Aβ42/40 are associated with worse clinical outcomes. p‐tau181 and Aβ42/40 are generally markers that are more specific to AD, while NfL and t‐tau are more general markers of neurodegeneration. p‐tau181, NfL, and t‐tau were log‐transformed prior to analyses. 2.6. Psychiatric and psychosocial functioning, health, and genetic risk Several measures were used to characterize the sample and were entered as covariates in the analyses. Depressive symptoms were assessed using the Geriatric Depression Scale (GDS). 31 In analyses, the GDS was included as a covariate, but six items that have been previously shown to load on a “cognitive impairment” factor (i.e., Feel you have more problems with memory than most?, Have trouble concentrating?, Your mind as clear as it used to be?, Frequently worry about the future?, Afraid that something bad is going to happen to you?, Easy for you to make decisions?) 32 were removed given the overlap with the SMCQ for a total GDS score range from 0 to 24. General worry symptoms were assessed with the Penn State Worry Questionnaire (PSWQ) to account for generalized worry not specific to memory concerns. 33 Vascular burden was captured using the sum of the dichotomous classifications (yes/no) of hypertension, dyslipidemia, diabetes, and cardiovascular disease (range = 0–4). Creatine levels were used to assess kidney function, which has been known to impact plasma ADRD biomarker levels. 34 Creatinine levels were log‐transformed prior to analyses. Apolipoprotein E ( APOE ) ε4 positivity was determined based on presence/absence of at least one ε4 allele. 2.7. Statistical analyses Participants were first descriptively characterized. Regression models were used to examine the associations of SMC with plasma biomarkers (p‐tau181, Aβ42/40, NfL, t‐tau). We examined a minimally adjusted model (Model 1) that included age, education, sex/gender, language of assessment (for H/L participant analyses), and depressive symptoms (minus the cognitive impairment items) given the known associations between SMC and depressive symptoms. 19 , 23 Next, additional covariates of symptoms of general worry, vascular burden, creatinine level, and APOE ε4 positivity were added to create a fully adjusted model (Model 2) to determine whether any associations of SMC with plasma biomarkers persisted after accounting for additional factors that may impact both SMC and plasma outcomes. False discovery rate (FDR)–corrected p values are presented for the primary plasma analyses. Given that the different racial/ethnic group samples have notably different ages, years of education, sex/gender distributions, baseline cognitive scores, and language backgrounds, all analyses were stratified by racial/ethnic group. Additional analyses examined the associations between SMC and objective memory as well as objective memory and plasma biomarkers using regression models. For these follow‐up models, the covariates were consistent with the Model 2 described above, but creatinine was only included if plasma markers were part of the model. Last, follow‐up analyses examined each of the four memory measures separately, rather than as a composite. 3. RESULTS 3.1. Participant characteristics Participants in the combined sample were on average 65.47 years of age, had 13.30 years of education, and were 64% female; however, there are notable differences across racial/ethnic group that support the use of stratified analyses. Table 1 shows the sociodemographic and clinical characteristics by racial/ethnic group. TABLE 1. Sociodemographic and clinical characteristic by racial/ethnic group. Hispanic/Latino ( n = 681) Non‐Hispanic Black ( n = 164) Non‐Hispanic White ( n = 773) Age 62.81 (7.73) 62.13 (7.15) 68.51 (8.34) Education 10.01 (4.52) 15.60 (2.68) 15.72 (2.56) Female/women, % 67.1% 74.4% 59.5% Assessed in Spanish, % 62.6% 0.0% 0.0% MMSE 26.96 (2.64) 28.54 (1.37) 29.19 (1.03) Income, $ 40803.14 (53961.80) 86403.11 (81291.27) 93862.33 (95646.95) SMCQ total 4.03 (3.28) 3.16 (2.79) 3.03 (2.55) Memory composite −0.02 (0.83) 0.17 (0.81) 0.02 (0.84) GDS total 5.97 (5.96) 5.27 (5.16) 4.22 (4.59) GDS (minus cognitive items) 3.92 (4.67) 3.57 (3.85) 2.84 (3.63) PSWQ total 38.78 (14.75) 37.48 (14.32) 38.64 (14.21) Vascular burden 1.75 (0.97) 1.75 (0.90) 1.46 (0.93) Creatinine (mg/dL) 0.80 (0.24) 0.94 (0.22) 0.91 (0.25) APOE ε4 genotype, % 23.5% 33.5% 22.9% p ‐tau181 1.78 (1.06) 1.76 (0.94) 2.21 (1.18) Aβ42/40 0.05 (0.01) 0.05 (0.02) 0.05 (0.01) NfL 15.26 (11.57) 10.70 (6.44) 17.53 (18.26) t‐tau 2.21 (0.79) 2.18 (0.80) 2.16 (0.88) Open in a new tab Note : Mean (standard deviation) reported unless otherwise indicated. Abbreviations: Aβ42/40, amyloid beta 42/40 ratio; APOE , apolipoprotein E; GDS, Geriatric Depression Scale; MMSE, Mini‐Mental State Examination; NfL, neurofilament light chain; p‐tau, phosphorylated tau; PSWQ, Penn State Worry Questionnaire; SMCQ, Subjective Memory Complaints Questionnaire; t‐tau, total tau. 3.2. Associations of SMC with plasma biomarkers 3.2.1. Minimally adjusted models General linear models examined the associations between SMC and AD/ADRD plasma biomarkers, stratified by racial/ethnic group. In the minimally adjusted Model 1, which adjusted for age, education, language of test administration (for the H/L group), and depressive symptoms (minus the cognitive items) as covariates, higher SMC was associated with higher p‐tau181 levels (β = 0.139, 95% confidence interval [CI: 0.057, 0.221], p < 0.001, η p 2 = 0.014) for NHW participants even after FDR correction ( p = 0.004), but not H/L (β = −0.011, 95% CI [−0.081, 0.059], p = 0.762, η p 2 < 0.001) or NHB (β = −0.021, 95% CI [−0.040, 0.138], p = 0.813, η p 2 < 0.001) participants. There was an incidental finding in this model such that higher depressive symptoms were associated with higher plasma p‐tau181 levels for NHB participants (β = 0.208, 95% CI [0.027, 0.389], p = 0.024, η p 2 = 0.032) that was slightly attenuated with FDR correction ( p = 0.094), but not for NHW (β = 0.006, 95% CI [−0.077, 0.088], p = 0.896, η p 2 < 0.001) or H/L (β = 0.052, 95% CI [−0.018, 0.122], p = 0.148, η p 2 = 0.003) participants. For the minimally adjusted Model 1, higher SMC was also associated with higher plasma NfL levels for NHW participants (β = 0.094, 95% CI [0.025, 0.163], p = 0.007, η p 2 = 0.010) even after FDR correction ( p = 0.014), but not H/L (β = 0.046, 95% CI [−0.026, 0.118], p = 0.208, η p 2 = 0.002) or NHB (β = 0.022, 95% CI [−0.148, 0.193], p = 0.796, η p 2 < 0.001) participants. There were no associations of SMC with Aβ42/40 or t‐tau across any of the racial/ethnic groups. Tables 2 , 3 , and 4 show the SMC and plasma associations for H/L, NHB, and NHW analyses, respectively. TABLE 2. Full models of associations between SMC and plasma ADRD biomarkers in Hispanic/Latino participants. p‐tau181 Aβ42/40 NfL t‐tau Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) SMC −0.011 (0.036) −0.016 (0.035) −0.012 (0.038) −0.008 (0.039) 0.046 (0.037) 0.029 (0.036) 0.011 (0.036) −0.004 (0.037) Age 0.342 (0.039) *** 0.280 (0.040) *** −0.128 (0.043) ** −0.085 (0.045) 0.533 (0.041) *** 0.455 (0.041) *** 0.122 (0.040) ** 0.070 (0.042) Education 0.072 (0.040) 0.053 (0.039) 0.066 (0.044) 0.065 (0.044) −0.028 (0.042) −0.045 (0.040) −0.013 (0.041) −0.035 (0.041) Female −0.069 (0.035) * 0.084 (0.042) * −0.097 (0.038) * −0.134 (0.046) ** 0.007 (0.036) 0.159 (0.042) *** 0.143 (0.036) *** 0.288 (0.043) *** Assessment in Spanish 0.005 (0.036) 0.029 (0.037) −0.005 (0.039) −0.013 (0.041) −0.029 (0.037) 0.011 (0.037) 0.078 (0.037) * −0.041 (0.038) GDS 0.052 (0.036) 0.050 (0.038) 0.013 (0.039) 0.018 (0.042) 0.068 (0.038) 0.046 (0.039) 0.061 (0.037) 0.038 (0.039) PSWQ — −0.033 (0.040) — 0.022 (0.045) — 0.006 (0.041) — 0.030 (0.042) Vascular burden 0 (reference) — — — — — 1 — −0.147 (0.121) — −0.041 (0.135) — −0.092 (0.123) — −0.102 (0.124) 2 — −0.094 (0.119) — −0.236 (0.133) — −0.018 (0.121) — −0.043 (0.123) 3 — 0.107 (0.130) — −0.358 (0.145) * — 0.357 (0.133) ** — 0.085 (0.134) 4 — 0.159 (0.265) — −0.273 (0.294) — 0.952 (264) *** — 0.096 (0.272) Creatinine — 0.260 (0.042) *** — −0.045 (0.047) — 0.244 (0.043) *** — 0.263 (0.044) *** APOE ε4 — −0.013 (0.035) — 0.016 (0.039) — 0.054 (0.035) — 0.005 (0.036) Adjusted R 2 0.109 0.164 0.022 0.035 0.236 0.305 0.045 0.099 Open in a new tab Abbreviations: Aβ42/40, amyloid beta 42/40 ratio; ADRD, Alzheimer's disease and related dementias; APOE , apolipoprotein E; GDS, Geriatric Depression Scale; NfL, neurofilament light chain; p‐tau, phosphorylated tau; PSWQ, Penn State Worry Questionnaire; SE, standard error; SMC, subjective memory concerns; t‐tau, total tau. * p < 0.05. ** p < 0.01. *** p < 0.001. TABLE 3. Full models of associations between SMC and plasma ADRD biomarkers in NHB participants. p‐tau181 Aβ42/40 NfL t‐tau Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) SMC −0.021 (0.090) 0.014 (0.091) 0.140 (0.136) 0.172 (0.146) 0.022 (0.087) 0.015 (0.087) −0.032 (0.095) −0.058 (0.096) Age 0.295 (0.085) *** 0.250 (0.090) ** −0.034 (0.128) −0.036 (0.142) 0.348 (0.081) *** 0.292 (0.087) ** −0.021 (0.090) −0.166 (0.095) Education 0.002 (0.120) −0.096 (0.121) 0.407 (0.184) * 0.357 (0.198) −0.128 (0.115) −0.203 (0.116) −0.019 (0.129) 0.032 (0.130) Female −0.190 (0.079) * −0.009 (0.094) 0.122 (0.124) 0.149 (0.152) 0.039 (0.075) −0.203 (0.116) * 0.399 (0.085) *** 0.578 (0.100) *** GDS 0.208 (0.091) * 0.253 (0.101) * −0.128 (0.144) −0.121 (0.165) 0.113 (0.087) 0.110 (0.098) 0.051 (0.097) 0.092 (0.106) PSWQ — −0.136 (0.090) — −0.026 (0.141) — −0.040 (0.088) — −0.112 (0.095) Vascular burden 0 (reference) — — — — — 1 — −0.131 (297) — −0.162 (0.479) — −0.280 (0.281) — −0.371 (0.324) 2 — −0.028 (0.298) — 0.027 (0.479) — −0.213 (0.282) — 0.032 (0.326) 3 — −0.133 (0.325) — −0.462 (0.534) — −0.151 (0.312) — 0.533 (0.355) 4 — −0.535 (0.554) — −0.219 (0.957) — −0.385 (0.577) — −0.045 (0.587) Creatinine — 0.343 (0.094) *** — 0.086 (0.148) — 0.349 (0.090) *** — 0.253 (0.099) * APOE ε4 — 0.050 (0.070) — 0.051 (0.112) — −0.049 (0.067) — −0.150 (0.074) * Adjusted R 2 0.097 0.162 0.022 0.003 0.102 0.160 0.105 0.157 Open in a new tab Abbreviations: Aβ42/40, amyloid beta 42/40 ratio; ADRD, Alzheimer's disease and related dementias; APOE , apolipoprotein E; GDS, Geriatric Depression Scale; NfL, neurofilament light chain; NHB, non‐Hispanic Black; p‐tau, phosphorylated tau; PSWQ, Penn State Worry Questionnaire; SE, standard error; SMC, subjective memory concerns; t‐tau, total tau. * p < 0.05. ** p < 0.01. *** p < 0.001. TABLE 4. Full models of associations between SMC and plasma ADRD biomarkers in NHW participants. p‐tau181 Aβ42/40 NfL t‐tau Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) Model 1 β (SE) Model 2 β (SE) SMC 0.139 (0.042) *** 0.109 (0.041) ** −0.002 (0.044) 0.005 (0.045) 0.094 (0.035) ** 0.056 (0.034) 0.009 (0.047) −0.026 (0.046) Age 0.378 (0.033) *** 0.367 (0.033) *** −0.183 (0.035) *** −0.181 (0.036) *** 0.495 (0.028) *** 0.471 (0.027) *** −0.002 (0.037) −0.038 (0.037) Education 0.054 (0.057) 0.043 (0.055) 0.030 (0.059) 0.034 (0.060) 0.039 (0.048) 0.038 (0.045) −0.076 (0.063) −0.060 (0.062) Female −0.112 (0.032) *** 0.024 (0.038) −0.002 (0.034) −0.020 (0.041) 0.004 (0.027) 0.169 (0.031) *** 0.212 (0.036) *** 0.375 (0.043) *** GDS 0.006 (0.042) −0.009 (0.044) −0.065 (0.044) −0.054 (0.048) 0.008 (0.035) 0.003 (0.036) 0.070 (0.047) 0.084 (0.050) PSWQ — 0.034 (0.037) — −0.021 (0.040) — 0.012 (0.030) — −0.042 (0.042) Vascular burden 0 (reference) — — — — 1 — −0.043 (0.097) — −0.028 (0.105) — −0.069 (0.079) — −0.103 (0.109) 2 — −0.085 (0.099) — −0.016 (0.106) — −0.079 (0.081) — −0.012 (0.111) 3 — −0.418 (0.132) ** — −0.014 (0.143) — −0.036 (0.108) — 0.332 (0.149) * 4 — 0.325 (0.250) — −0.213 (269) — 0.226 (204) — 0.244 (0.281) Creatinine — 0.301 (0.042) *** — −0.041 (0.045) — 0.326 (0.034) *** — 0.281 (0.047) *** APOE ε4 — −0.003 (0.033) — −0.061 (0.036) — −0.052 (0.027) — −0.017 (0.038) Adjusted R 2 0.173 0.224 0.038 0.032 0.306 0.381 0.050 0.097 Open in a new tab Abbreviations: Aβ42/40, amyloid beta 42/40 ratio; ADRD, Alzheimer's disease and related dementias; APOE , apolipoprotein E; GDS, Geriatric Depression Scale; NfL, neurofilament light chain; NHW, non‐Hispanic White; p‐tau, phosphorylated tau; PSWQ, Penn State Worry Questionnaire; SE, standard error; SMC, subjective memory concerns; t‐tau, total tau. * p < 0.05. ** p < 0.01. *** p < 0.001. 3.2.2. Fully adjusted models In the fully adjusted Model 2 that included the covariates in Model 1 plus general worry symptom severity, vascular burden, creatinine, and APOE ε4 carrier status, higher SMC was still associated with higher p‐tau181 levels (β = 0.109, 95% CI [0.028, 0.190], p = 0.008, η p 2 = 0.009) for NHW participants even after FDR correction ( p = 0.032), but not H/L (β = −0.016, 95% CI [−0.086, 0.054], p = 0.654, η p 2 < 0.001) or NHB (β = 0.014, 95% CI [−0.166, 0.194], p = 0.879, η p 2 < 0.001) participants (see Figure 1A ). The incidental finding showing that higher depressive symptoms were associated with higher plasma p‐tau181 levels for NHB participants persisted in this fully adjusted model (β = 0.253, 95% CI [0.054, 0.453], p = 0.013, η p 2 = 0.040) though this was slightly attenuated after FDR correction ( p = 0.052), but remained non‐significant for NHW and H/L participants (Figure 1B ). For the fully adjusted Model 2, higher SMC was no longer associated with higher plasma NfL levels (β = 0.056, 95% CI [−0.011, 0.122], p = 0.099, η p 2 = 0.004) for NHW participants, and there was no association for H/L and NHB participants. Again, there were no associations of SMC with Aβ42/40 or t‐tau across any of the racial/ethnic groups. FIGURE 1. Open in a new tab Associations of subjective memory concerns (A) and depressive symptoms (B) with plasma p‐tau181 by racial/ethnic group. GDS, Geriatric Depression Scale; H/L, Hispanic/Latino; NHB, non‐Hispanic Black; NHW, non‐Hispanic White; p‐tau, phosphorylated tau. 3.3. Exploratory associations of SMC with objective memory Next, models exploring the associations between SMC and objective memory performance were conducted that adjusted for age, education, sex/gender, language of assessment (for H/L participant analyses), depressive symptoms (minus the cognitive impairment items), general worry, vascular burden, and APOE ε4 positivity. Results show that higher SMC are associated with lower objective memory performance for H/L (β = −0.106, 95% CI [−0.168, −0.045], p < 0.001, η p 2 = 0.015) and NHW (β = −0.134, 95% CI [−0.209, −0.059], p < 0.001, η p 2 = 0.014) participants, but not NHB participants (β = −0.020, 95% CI [−0.163, 0.123], p = 0.781, η p 2 < 0.001; see Figure 2 ). The pattern of results was largely unchanged when the individual measures from the memory composite were included as the outcome (Table S1 in supporting information), though associations were stronger for the SEVLT scores compared to the Logical Memory scores. FIGURE 2. Open in a new tab Association between subjective memory concerns and objective memory performance by racial/ethnic group. H/L, Hispanic/Latino; NHB, non‐Hispanic Black; NHW, non‐Hispanic White. 3.4. Exploratory associations of objective memory with plasma biomarkers Finally, secondary models examining the association between objective memory performance and AD/ADRD plasma biomarkers were conducted that adjusted for age, education, sex/gender, language of assessment (for H/L participant analyses), depressive symptoms (minus the cognitive impairment items), general worry, vascular burden, and APOE ε4 positivity. Notably, the objective memory composite score was not associated with any of the AD/ADRD plasma biomarker levels across any of the racial/ethnic groups ( p values range = 0.121–0.930). When exploring the individual memory scores included in the composite, the pattern of results was largely the same with minimal significant associations (Table S2 in supporting information). However, for the model examining the association of the SEVLT delayed recall with plasma NfL and t‐tau, there were now effects for the H/L group such that lower SEVLT delayed recall was associated with higher levels of NfL (β = −0.086, 95% CI [−0.165, −0.007], p = 0.033, η p 2 = 0.007) and t‐tau (β = −0.096, 95% CI [−0.176, −0.015], p = 0.020, η p 2 = 0.008). Within NHW participants, there were associations of SEVLT immediate recall (β = −0.073, 95% CI [−0.145, −0.001], p = 0.048, η p 2 = 0.005) and delayed recall (β = −0.093, 95% CI [−0.162, −0.025], p = 0.008, η p 2 = 0.009) with plasma p‐tau181 only. There were no associations of immediate and delayed recall on Logical Memory with any plasma biomarkers as well as no associations for any of the individual measures with any plasma biomarkers within NHB participants. 4. DISCUSSION Our study showed that within CU participants in HABS‐HD, racial/ethnic groups demonstrate different patterns of associations between subjective memory and plasma ADRD biomarkers. Specifically, higher SMC were associated with higher plasma p‐tau181 and NfL (in minimally adjusted models) in NHW participants, but not in H/L or NHB participants. Further, higher SMC were associated with lower objective memory performance in NHW and H/L participants, but not NHB participants. There was no association between the objective memory composite and plasma biomarkers across any of the three racial/ethnic groups, though examination of the individual memory test scores demonstrated a different pattern with the SEVLT and plasma biomarkers for H/L and NHW participants. Interestingly, an incidental finding showed that higher depressive symptoms were associated with higher plasma p‐tau181 in NHB participants only, though this finding was slightly attenuated after FDR correction. Results suggest that the utility of SMC as an early indicator of AD‐related changes may vary across racial/ethnic groups and specific outcomes of interest. While SMC were associated with plasma biomarkers for NHW participants only, SMC were associated with objective memory performance for both H/L and NHW participants. From a biological perspective, results suggest mechanisms beyond AD may be associated with subtle cognitive changes in H/L older adults because there was not an association with AD plasma biomarkers, and that the utility of SMC as an indicator of AD‐specific pathologic change within this group may be more limited. Studies have shown that cerebrovascular pathology is more prevalent in H/L than NHW older adults. 35 , 36 Thus, we expected SMC to be associated with NfL in H/L older adults given NfL is a more general marker of neurodegeneration that may change due to mechanisms beyond AD, including cerebrovascular disease. 37 , 38 However, even in the minimally adjusted model that didn't include vascular risk burden as a covariate, there was only an association between SMC and NfL for NHW, rather than H/L older adults. Future work should explore whether more sensitive markers of cerebrovascular or other biological processes including inflammation may be more closely linked to SMC in H/L and NHB older adults. Alternatively, it is possible that other psychosocial and cultural factors may be more directly associated with SMC, rather than AD/ADRD or neurodegenerative plasma biomarkers. For example, within H/L older adults, prior work has shown no association between SCD and objective cognition after adjusting for depressive symptoms, and depressive symptoms related to SCD even after adjusting for objective cognition. 19 Prior work that included NHB and H/L participants from HABS‐HD showed an association between SMC and participants with low socioeconomic and social resources and higher depression and worry symptoms. 39 Further, preliminary work in Mexican Americans from HABS‐HD showed that higher chronic stress and lower social support were associated with greater SMC. 40 In our follow‐up analyses examining the association between individual objective memory tests and plasma outcomes, within H/L older adults, the SEVLT delayed recall was associated with plasma markers of neurodegeneration (NfL and t‐tau), but not more AD‐specific markers (p‐tau, Aβ42/40). These small associations suggest that even in CU older adults, subtle objective memory difficulties are associated with neurodegeneration outcomes. The fact that SMC did not show this association with plasma outcomes within H/L participants may suggest that SMC may be more tightly linked with psychosocial factors (e.g., economic and social resources, stress) in this group such that assessment of individual and neighborhood‐level psychosocial and cultural factors in tandem with biomarker characterization may be particularly important in clinical assessments. More work is needed to better understand specific psychosocial and sociocultural factors that are most tightly linked to SMC, which is likely to vary both across as well as within racial/ethnic groups. Within NHB participants, SMC were not related to AD/ADRD plasma biomarkers or objective memory. The lack of association of objective memory was unexpected as there was a significant association for both H/L and NHW participants. However, the literature is mixed such that while some prior work has shown the utility of subjective concerns for predicting progression to cognitive impairment in Black/African American older adults, 21 other studies have shown that SMC may not be associated with objective cognition or incident cognitive impairment in Black/African American older adults. 15 , 41 , 42 Notably, NHB participants in HABS‐HD are fairly young (mean age = 62 years) and had the highest mean objective memory composite relative to H/L and NHW groups, which suggests SMC and objective memory associations may be weaker in younger, higher performing groups. Furthermore, this group also had a very high proportion of women (75%), who have a known verbal memory advantage. 43 , 44 Therefore, it is possible that the lack of association between SMC and objective memory performance may be due to largely preserved high level of objective memory within CU NHB participants in HABS‐HD. Furthermore, the NHB group was also the smallest sample size, so it is possible that the power to detect small effects in this group was limited. Past work has found associations between SMC and depressive symptoms in NHB participants, suggesting mood symptoms may better predict SMC than AD/ADRD plasma biomarkers or objective memory. 16 , 20 Within this study, there was a small association that emerged between depressive symptoms and plasma p‐tau181 within NHB participants. Prior work has demonstrated that mood or neuropsychiatric symptoms may be important early symptoms of AD pathogenesis. 45 It is possible that in a high functioning group, mood symptoms might be a particularly early sign of AD‐related biomarker changes, even prior to changes in subjective or objective memory performance. Further work is needed to also explore the role of sex and early neuropsychiatric symptoms, given the verbal memory advantage in women might delay the ability to detect subtle changes in cognition. 46 , 47 A significant strength of the current study includes the availability of plasma AD/ADRD biomarkers across three racial/ethnic groups recruited from the community. To our knowledge, the association of SMC with plasma AD/ADRD biomarkers has not yet been examined across a diverse sample of older adults. Limitations of the current study include the cross‐sectional design. It is possible that while SMC may only have small associations cross‐sectionally, that they are still prognostically useful for determining progression to MCI or dementia as well as predictive of future increases in AD/ADRD biomarkers. 9 , 10 , 21 Additionally, the focus on SMC and objective memory performance in this study did not explore other domains such as executive function that may be more affected across non‐White racial/ethnic groups. Future research should explore other AD biomarker associations with SMC (e.g., amyloid and tau PET), other non‐AD mechanisms (e.g., inflammation), and how social and structural determinants of health may both impact overall SMC and moderate the association of SMC with AD‐related outcomes within race/ethnicity groups. Taken together, results highlight different patterns of associations among subjective memory, objective memory, and plasma AD/ADRD biomarkers within racial/ethnic groups. While SMC may be an early indicator of AD/ADRD‐related changes in NHW and objective memory performance in H/L and NHW participants, these associations were relatively small and suggest that alternative mechanisms are likely contributing to one's subjective evaluation of memory functioning. Results contribute to the literature suggesting that SMC may be useful for early detection, but that more work is needed to develop a more comprehensive and personalized approach to early AD/ADRD detection among diverse older adults. CONFLICT OF INTEREST STATEMENT S.E.O. is founding scientist of Cx Precision Medicine and owns equity and is a senior associate editor at Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring . He also has served on advisory boards for Eisai and Quanterix. Other authors report no disclosures. Author disclosures are available in the supporting information . CONSENT STATEMENT The HABS‐HD study protocol is conducted under the University of North Texas Health Science Center, Institutional Review Board approval. Each HABS‐HD participant (and/or legal guardian) provides a signed written informed consent to participate in the study. Supporting information Supporting Information DAD2-18-e70324-s001.pdf (607.6KB, pdf) Supporting Information DAD2-18-e70324-s002.docx (22.7KB, docx) ACKNOWLEDGMENTS The authors thank the Health and Aging Brain Study‐Health Disparities (HABS‐HD) research team and participants. This project was supported by the Alzheimer's Association (AARG‐22‐723000) and NIH/NIA (RF1 AG082726). HABS‐HD is supported by the NIH/NIA under Award Numbers R01AG054073 and R01AG058533, P41EB015922, and U19AG078109. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. HABS‐HD Study Team Sid E. O'Bryant, Kristine Yaffe, Arthur Toga, Robert Rissman, & Leigh Johnson; and the HABS‐HD Investigators: Meredith Braskie, Kevin King, James R. Hall, Melissa Petersen, Raymond Palmer, Robert Barber, Yonggang Shi, Fan Zhang, Rajesh Nandy, Roderick McColl, David Mason, Bradley Christian, Nicole Phillips, Stephanie Large, Joe Lee, Badri Vardarajan, Monica Rivera Mindt, Amrita Cheema, Lisa Barnes, Mark Mapstone, Annie Cohen, Amy Kind, Ozioma Okonkwo, Raul Vintimilla, Zhengyang Zhou, Michael Donohue, Rema Raman, Matthew Borzage, Michelle Mielke, Beau Ances, Ganesh Babulal, Jorge Llibre‐Guerra, Carl Hill, and Rocky Vig. Thomas KR, Terao CM, Weigand AJ, Petersen M, O'Bryant S, Clark AL. Subjective memory concerns and AD/ADRD plasma biomarker associations in HABS‐HD. Alzheimer's Dement. 2026;18:e70324. 10.1002/dad2.70324 See HABS‐HD Study Team in the Acknowledgments section. Contributor Information Kelsey R. Thomas, Email: [email protected]. HABS‐HD Study Team: Sid E. O'Bryant , Kristine Yaffe , Arthur Toga , Robert Rissman , Leigh Johnson , Meredith Braskie , Kevin King , James R. Hall , Melissa Melissa Petersen , Raymond Palmer , Robert Barber , Yonggang Shi , Fan Zhang , Rajesh Nandy , Roderick McColl , David Mason , Bradley Christian , Nicole Phillips , Stephanie Large , Joe Lee , Badri Vardarajan , Monica Rivera Mindt , Amrita Cheema , Lisa Barnes , Mark Mapstone , Annie Cohen , Amy Kind , Ozioma Okonkwo , Raul Vintimilla , Zhengyang Zhou , Michael Donohue , Rema Raman , Matthew Borzage , Michelle Mielke , Beau Ances , Ganesh Babulal , Jorge Llibre‐Guerra , Carl Hill , and Rocky Vig DATA AVAILABILITY STATEMENT All data used in this manuscript are publicly available to the qualified researchers at https://apps.unthsc.edu/itr/ . REFERENCES 1. Sperling RA, Rentz DM, Johnson KA, et al. The A4 study: stopping AD before symptoms begin? Sci Transl Med. 2014;6(228):228fs13. doi: 10.1126/scitranslmed.3007941 [ Google Scholar ] 2. 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Nat Rev Neurol. 2018;14(8):457‐469. doi: 10.1038/s41582‐018‐0032‐9 [ DOI ] [ PubMed ] [ Google Scholar ] Associated Data This section collects any data citations, data availability statements, or supplementary materials included in this article. Supplementary Materials Supporting Information DAD2-18-e70324-s001.pdf (607.6KB, pdf) Supporting Information DAD2-18-e70324-s002.docx (22.7KB, docx) Data Availability Statement HABS‐HD is a single‐site community‐based research study that seeks to understand ADRD risk in racially/ethnically diverse older adults that reside in the Dallas and Fort Worth, Texas metropolitan area. 24 HABS‐HD data are publicly available and consist of cognitive, behavioral, clinical lab, blood plasma, brain magnetic resonance imaging (MRI) and PET scans assessments. Written informed consent was obtained for all study participants and HABS‐HD was approved by the University of North Texas Health Science Center Institutional Review Board. Data from HABS‐HD release 3 were used to maximize the number of available participants in which the same plasma biomarker assay was used for phosphorylated tau 181 (p‐tau181). All data used in this manuscript are publicly available to the qualified researchers at https://apps.unthsc.edu/itr/ . 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