Limited early IVIG for the treatment of pediatric myelin oligodendrocyte glycoprotein antibody-associated disease
(2025) Multiple Sclerosis and Related Disorders, 97, art. no. 106345, .
MacRae, R.a , Race, J.b , Schuette, A.b , Waltz, M.b , Casper, T.C.b , Rose, J.b , Abrams, A.c , Rensel, M.c , Waubant, E.d , Virupakshaiah, A.d , Schoeps, V.d , O’Neill, K.e , Ness, J.f , Wheeler, Y.f , Shukla, N.g , Mar, S.h , Rodriguez, M.i , Chitnis, T.j , Gorman, M.a , Benson, L.a
a Boston Children’s Hospital, Harvard Medical SchoolMA, United States
b The University of UtahUT, United States
c Cleveland Clinic, Cleveland, OH, United States
d UCSF Weill Institute for Neurosciences, San Francisco, CA, United States
e NYU Langone Medical Center, New York, NY, United States
f Children’s of Alabama, Birmingham, AL, United States
g Texas Children’s Hospital, Houston, TX, United States
h Washington University in St Louis, St Louis, MO, United States
i Mayo Clinic Rochester, Rochester, MN, United States
j Massachusetts General Hospital, Boston, MA, United States
Abstract
Background and Objectives: This study aimed to evaluate whether a 6-month (limited) course of early IVIG is an effective strategy for relapse prevention in children with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) versus only acute therapies or other early immunotherapies. Methods: This was a retrospective multicenter observational study of pediatric MOGAD patients from the US Network of Pediatric Multiple Sclerosis Centers with disease onset between October 1996 and December 2022. Controls were matched to limited early IVIG subjects using a 3:1 ratio. Hazard ratios of time to relapse and rate ratios of annualized relapse rate were calculated. The cumulative probability of remaining relapse-free was evaluated with the Kaplan-Meier method. Results: We identified 130 unique control subjects treated before second attack with acute treatments only used in matching, 18 subjects treated with limited early IVIG, and 23 subjects treated with other early immunotherapy. The time to relapse was not different between either the limited early IVIG group and control group (HR 0.60 [0.22, 1.66], p = 0.32) or other early immunotherapy group (HR 0.98 [0.27, 3.6], p = 0.98). The limited early IVIG group showed a lower annualized relapse rate, although not statistically significant (RR 0.44 [0.17, 1.14], p = 0.09) compared with controls and a similar annualized relapse rate compared with the other early immunotherapy group (RR 0.56 [0.19, 1.69], p = 0.30). Discussion: Although underpowered, our results suggest that the use of a limited, 6-month course of early IVIG may reduce the risk of multiphasic disease in pediatric MOGAD. © 2025 Elsevier B.V.
Author Keywords
Immunotherapy; MOG; MOGAD; Pediatric; Relapse
Document Type: Article
Publication Stage: Final
Source: Scopus
Genetically Engineered Brain Organoids Recapitulate Spatial and Developmental States of Glioblastoma Progression
(2025) Advanced Science, 12 (10), art. no. 2410110, .
Ishahak, M.a , Han, R.H.b , Annamalai, D.b , Woodiwiss, T.c , McCornack, C.b , Cleary, R.T.b , DeSouza, P.A.b , Qu, X.b , Dahiya, S.d , Kim, A.H.b e f , Millman, J.R.a g
a Division of Endocrinology, Metabolism and Lipid Research, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8127, St. Louis, MO 63110, United States
b Department of Genetics, Washington University School of Medicine, 4515 McKinley Ave., St. Louis, MO 63110, United States
c Department of Neurological Surgery, University of Iowa Healthcare, 1800 John Pappajohn Pavilion, Iowa City, IA 52242, United States
d Division of Neuropathology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8118, St. Louis, MO 63110, United States
e Taylor Family Department of Neurosurgery, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8057, St. Louis, MO 63110, United States
f The Brain Tumor Center at Siteman Cancer Center, 4921 Parkview Place, St. Louis, MO 63110, United States
g Department of Biomedical Engineering, Washington University, 1 Brookings Drive, Campus Box 1097, St. Louis, MO 63130, United States
Abstract
Glioblastoma (GBM) is an aggressive form of brain cancer that is highly resistant to therapy due to significant intra-tumoral heterogeneity. The lack of robust in vitro models to study early tumor progression has hindered the development of effective therapies. Here, this study develops engineered GBM organoids (eGBOs) harboring GBM subtype-specific oncogenic mutations to investigate the underlying transcriptional regulation of tumor progression. Single-cell and spatial transcriptomic analyses revealed that these mutations disrupt normal neurodevelopment gene regulatory networks resulting in changes in cellular composition and spatial organization. Upon xenotransplantation into immunodeficient mice, eGBOs form tumors that recapitulate the transcriptional and spatial landscape of human GBM samples. Integrative single-cell trajectory analysis of both eGBO-derived tumor cells and patient GBM samples reveal the dynamic gene expression changes in developmental cell states underlying tumor progression. This analysis of eGBOs provides an important validation of engineered cancer organoid models and demonstrates their utility as a model of GBM tumorigenesis for future preclinical development of therapeutics. © 2025 The Author(s). Advanced Science published by Wiley-VCH GmbH.
Author Keywords
brain organoids; genetic engineering; glioblastoma; single-cell RNA sequencing; spatial sequencing
Funding details
Alvin J. Siteman Cancer CenterSCC
Edward Mallinckrodt, Jr. FoundationEMF
National Center for Research ResourcesNCRR
Mallinckrodt Institute of Radiology, School of Medicine, Washington University in St. LouisMIR
University of WashingtonUWS10OD026913
University of WashingtonUW
National Cancer InstituteNCIP30CA91842
National Cancer InstituteNCI
Foundation for Barnes-Jewish HospitalFBJHR25 NS090978, T32DK007120
Foundation for Barnes-Jewish HospitalFBJH
National Institutes of HealthNIHR01 NS106612, R01 NS094670, R01 NS128470
National Institutes of HealthNIH
American Cancer SocietyACSPF‐21‐149‐01‐CDP
American Cancer SocietyACS
Document Type: Article
Publication Stage: Final
Source: Scopus
Autism- and intellectual disability-associated MYT1L mutation alters human cortical interneuron differentiation, maturation, and physiology
(2025) Stem Cell Reports, 20 (3), art. no. 102421, .
Prakasam, R.a , Determan, J.a , Chapman, G.a , Narasimhan, M.a , Shen, R.a , Saleh, M.a , Kaushik, K.a , Gontarz, P.a , Meganathan, K.a , Hakim, B.a , Zhang, B.a , Huettner, J.E.b , Kroll, K.L.a
a Department of Developmental Biology, Washington University School of Medicine, St Louis, MO 63110, United States
b Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, United States
Abstract
Myelin transcription factor 1 like (MYT1L) is a neuronal transcription factor highly expressed in the developing and adult brain, and, while pathogenic MYT1L mutations cause neurodevelopmental disorders, these have not been characterized in human models of neurodevelopment. Here, we modeled the consequences of pathogenic MYT1L mutation using human stem cell-derived cortical neurons, demonstrating that MYT1L mutation alters the differentiation trajectory, increasing neuronal gene expression, morphological complexity, and synapse production. We also examined consequences of MYT1L mutation in mature cortical interneurons, identifying hallmarks of impaired neuronal identity and maturation and correspondingly altered channel expression and electrophysiological properties. Finally, by defining MYT1L genome-wide occupancy in cortical interneurons, we identified direct MYT1L targets likely to mediate these phenotypes. Together, this work elucidates new MYT1L requirements for human cortical interneuron development and demonstrates how pathogenic MYT1L mutation perturbs this developmental program, contributing to the etiology of neurodevelopmental disorders. © 2025 The Author(s)
Author Keywords
ASD; autism spectrum disorder; cIN; human cortical interneuron; human pluripotent stem cell; MYT1L; NDDs; neurodevelopmental disorders
Funding details
School of Medicine, Washington University in St. LouisWUSM
Genome Technology Access CenterGTAC
LI-2019-8-19
National Institutes of HealthNIHP50HD103525, R01HD110556, R01MH124808, R01NS114551
National Institutes of HealthNIH
Document Type: Article
Publication Stage: Final
Source: Scopus
Accuracy and Longitudinal Consistency of PET/MR Attenuation Correction in Amyloid PET Imaging amid Software and Hardware Upgrades
(2025) American Journal of Neuroradiology, 46 (3), pp. 635-642.
Ying, C.a , Chen, Y.b , Yan, Y.c , Flores, S.a , Laforest, R.a , Benzinger, T.L.S.a c d e , An, H.a b
a Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, United States
b Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
c Department of Surgery, Washington University School of Medicine, St. Louis, MO, United States
d Department of Neurosurgery, Washington University School of Medicine, St. Louis, MO, United States
e Knight Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO, United States
Abstract
BACKGROUND AND PURPOSE: Integrated PET/MR allows the simultaneous acquisition of PET biomarkers and structural and functional MRI to study Alzheimer disease (AD). Attenuation correction (AC), crucial for PET quantification, can be performed by using a deep learning approach, DL-Dixon, based on standard Dixon images. Longitudinal amyloid PET imaging, which provides important information about disease progression or treatment responses in AD, is usually acquired over several years. Hardware and software upgrades often occur during a multiple-year study period, resulting in data variability. This study aims to harmonize PET/MR DL-Dixon AC amid software and head coil updates and evaluate its accuracy and longitudinal consistency. MATERIALS AND METHODS: Tri-modality PET/MR and CT images were obtained from 329 participants, with a subset of 38 undergoing tri-modality scans twice within approximately 3 years. Transfer learning was used to fine-tune DL-Dixon models on images from 2 scanner software versions (VB20P and VE11P) and 2 head coils (16-channel and 32-channel coils). The accuracy and longitudinal consistency of the DL-Dixon AC were evaluated. Power analyses were performed to estimate the sample size needed to detect various levels of longitudinal changes in the PET standardized uptake value ratio (SUVR). RESULTS: The DL-Dixon method demonstrated high accuracy across all data, irrespective of scanner software versions and head coils. More than 95.6% of brain voxels showed less than 10% PET relative absolute error in all participants. The median [interquartile range] PET mean relative absolute error was 1.10% [0.93%, 1.26%], 1.24% [1.03%, 1.54%], 0.99% [0.86%, 1.13%] in the cortical summary region, and 1.04% [0.83%, 1.36%], 1.08% [0.84%, 1.34%], 1.05% [0.72%, 1.32%] in cerebellum by using the DL-Dixon models for the VB20P 16-channel coil, VE11P 16-channel coil, and VE11P 32-channel coil data, respectively. The within-subject coefficient of variation and intraclass correlation coefficient of PET SUVR in the cortical regions were comparable between the DL-Dixon and CT AC. Power analysis indicated that similar numbers of participants would be needed to detect the same level of PET changes by using DL-Dixon and CT AC. CONCLUSIONS: DL-Dixon exhibited excellent accuracy and longitudinal consistency across the 2 software versions and head coils, demonstrating its robustness for longitudinal PET/MR neuroimaging studies in AD. © 2025 American Society of Neuroradiology. All rights reserved.
Document Type: Article
Publication Stage: Final
Source: Scopus
Spatial histomorphometry reveals that local peripheral nerves modulate but are not required for skeletal adaptation to applied load in mice
(2025) JBMR Plus, 9 (3), art. no. ziaf006, .
Beeve, A.T.a b , Hassan, M.G.b , Li, A.b , Migotsky, N.a c , Silva, M.J.c , Scheller, E.L.a b
a Department of Biomedical Engineering, Washington University, St. Louis, MO 63130, United States
b Department of Medicine, Division of Bone and Mineral Diseases, Washington University, St. Louis, MO 63110, United States
c Department of Orthopaedics, Washington University, St. Louis, MO 63110, United States
Abstract
Mechanical loading is required for bone health and results in skeletal adaptation to optimize strength. Local nerve axons, particularly within the periosteum, may respond to load-induced biomechanical and biochemical cues. However, their role in the bone anabolic response remains controversial. We hypothesized that spatial alignment of periosteal nerves with sites of load-induced bone formation would clarify this relationship. To achieve this, we developed RadialQuant, a custom tool for spatial histomorphometry. Tibiae of control and neurectomized (sciatic/femoral nerve cut) pan-neuronal Baf53b-tdTomato reporter mice were loaded for 5 days. Bone formation and periosteal nerve axon density were then quantified simultaneously in non-decalcified sections of the mid-diaphysis using RadialQuant. In control animals, anabolic loading induced maximal periosteal bone formation at the site of peak compression, as has been reported previously. By contrast, loading did not significantly change overall periosteal nerve density. Neurectomy depleted ∼90% of all periosteal axons, with near-total depletion on load-responsive surfaces. Neurectomy alone also caused de novo bone formation on the lateral aspect of the mid-diaphysis. However, neurectomy did not inhibit load-induced increases in periosteal bone area, mineralizing surface, or bone formation rate. Rather, neurectomy spatially redistributed load-induced bone formation toward the lateral tibial surface with a reduction in periosteal bone formation at the posterolateral apex (-63%) and enhancement at the lateral surface (+1360%). Altogether, this contributed to comparable load-induced changes in cortical bone area fraction. Our results show that local skeletal innervation modulates but is not required for skeletal adaptation to applied load in our model. This supports the continued use of loading and weight-bearing exercise as an effective strategy to increase bone mass, even in settings of peripheral nerve damage or dysfunction. © 2025 The Author(s).
Author Keywords
biomechanical loading; biomechanics; bone histomorphometry; bone-brain-nervous system interactions; interoception; osteoblasts; sensory nerve
Funding details
Center for Cellular Imaging, Washington UniversityWUCCI
Center of Regenerative Medicine, Washington University in St. LouisCRM, WUSTL
National Institutes of HealthNIHR21-AR079052, T32-AR060719, R01-DK132073, R01-AR047867, F31-AR081123, R21-DE032420
National Institutes of HealthNIH
Musculoskeletal Research Center, Washington University in St. LouisMRCP30-AR074992
Musculoskeletal Research Center, Washington University in St. LouisMRC
Document Type: Article
Publication Stage: Final
Source: Scopus
Notch inhibition enhances morphological reprogramming of microRNA-induced human neurons
(2025) Stem Cells, 43 (2), art. no. sxae079, .
Burbach, K.F.a b , Wu, S.a b , Yoo, A.S.a c
a Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, United States
b Program in Molecular Genetics and Genomics, Division of Biology & Biomedical Sciences, Washington University in St. Louis, St. Louis, MO 63110, United States
c Center for Regenerative Medicine, Washington University in St. Louis, St. Louis, MO 63110, United States
Abstract
The role of Notch signaling in direct neuronal reprogramming remains unknown despite its importance to brain development in vivo. Here, we use microRNA-induced neurons that are directly reprogrammed from human fibroblasts to determine how Notch signaling contributes to neuronal identity. We found that Notch inhibition during the first week of reprogramming was both necessary and sufficient to enhance neurite outgrowth at a later timepoint, indicating an important role in the erasure of the original cell identity. Accordingly, transcriptomic analysis showed that the effect of Notch inhibition was likely due to improvements in fibroblast fate erasure and silencing of non-neuronal genes. To this effect, we identify MYLIP, whose downregulation in response to Notch inhibition significantly promoted neurite outgrowth. Moreover, Notch inhibition resulted in cells with neuronal transcriptome signatures defined by expressing long genes at a faster rate than the control, demonstrating the effect of accelerated fate erasure on neuronal fate acquisition. Our results demonstrate the antagonistic role of Notch signaling to the pro-neuronal microRNAs 9 and 124 and the benefits of its inhibition to the acquisition of neuronal morphology. © 2024 The Author(s). Published by Oxford University Press. All rights reserved.
Author Keywords
direct cell reprogramming techniques; microRNAs; MYLIP; notch
Funding details
National Institutes of HealthNIH
Genome Technology Access CenterGTAC
National Center for Research ResourcesNCRR
Cure Alzheimer’s FundCAF
National Cancer InstituteNCI#P30 CA91842
National Cancer InstituteNCI
National Institute on AgingNIARF1AG056296
National Institute on AgingNIA
National Institute of Neurological Disorders and StrokeNINDSR01NS107488, R01AG0789640
National Institute of Neurological Disorders and StrokeNINDS
Document Type: Article
Publication Stage: Final
Source: Scopus
A cryptic pocket in CB1 drives peripheral and functional selectivity
(2025) Nature, art. no. 107847, .
Rangari, V.A.a b , O’Brien, E.S.c j , Powers, A.S.c d e f , Slivicki, R.A.b , Bertels, Z.b , Appourchaux, K.a b , Aydin, D.c d e f , Ramos-Gonzalez, N.a b , Mwirigi, J.b , Lin, L.g , Mangutov, E.a b , Sobecks, B.L.c d e f , Awad-Agbaria, Y.a b , Uphade, M.B.a b , Aguilar, J.a b , Peddada, T.N.c , Shiimura, Y.c h , Huang, X.-P.i , Folarin-Hines, J.b , Payne, M.b , Kalathil, A.a , Varga, B.R.a b , Kobilka, B.K.d , Pradhan, A.A.a b , Cameron, M.D.g , Kumar, K.K.d , Dror, R.O.c d e f , Gereau, R.W., IVa b , Majumdar, S.a b
a Center for Clinical Pharmacology, University of Health Sciences and Pharmacy and Washington University School of Medicine, St. Louis, MO, United States
b Department of Anesthesiology and Washington University Pain Center, Washington University School of Medicine, St. Louis, MO, United States
c Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, United States
d Department of Computer Science, Stanford University, Stanford, CA, United States
e Department of Structural Biology, Stanford University School of Medicine, Stanford, CA, United States
f Institute for Computational and Mathematical Engineering, Stanford University, Stanford, CA, United States
g Department of Molecular Medicine, UF Scripps Biomedical Research, Jupiter, FL, United States
h Division of Molecular Genetics, Institute of Life Science, Kurume University, Fukuoka, Japan
i Department of Pharmacology School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States
j Department of Biophysics and Biophysical Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD, United States
Abstract
The current opioid overdose epidemic highlights the urgent need to develop safer and more effective treatments for chronic pain1. Cannabinoid receptor type 1 (CB1) is a promising non-opioid target for pain relief, but its clinical use has been limited by centrally mediated psychoactivity and tolerance. We overcame both issues by designing peripherally restricted CB1 agonists that minimize arrestin recruitment. We achieved these goals by computationally designing positively charged derivatives of the potent CB1 agonist MDMB-Fubinaca2. We designed these ligands to occupy a cryptic pocket identified through molecular dynamics simulations—an extended binding pocket that opens rarely and leads to the conserved signalling residue D2.50 (ref. 3). We used structure determination, pharmacological assays and molecular dynamics simulations to verify the binding modes of these ligands and to determine the molecular mechanism by which they achieve this dampening of arrestin recruitment. Our lead ligand, VIP36, is highly peripherally restricted and demonstrates notable efficacy in three mouse pain models, with 100-fold dose separation between analgesic efficacy and centrally mediated side effects. VIP36 exerts analgesic efficacy through peripheral CB1 receptors and shows limited analgesic tolerance. These results show how targeting a cryptic pocket in a G-protein-coupled receptor can lead to enhanced peripheral selectivity, biased signalling, desired in vivo pharmacology and reduced adverse effects. This has substantial implications for chronic pain treatment but could also revolutionize the design of drugs targeting other G-protein-coupled receptors. © The Author(s), under exclusive licence to Springer Nature Limited 2025.
Funding details
Pharmaceutical Research and Manufacturers of America FoundationPhRMAFPhRMA Foundation, 0000 0000 9959 8153
Pharmaceutical Research and Manufacturers of America FoundationPhRMAF
National Institutes of HealthNIHK99DA056691, R34NS126036, F32DA051160
National Institutes of HealthNIH
National Institute of Mental HealthNIMHHHSN-271-2018-00023-C
National Institute of Mental HealthNIMH
Document Type: Article
Publication Stage: Article in Press
Source: Scopus
Characterization of plasma AT(N) biomarkers among a racial and ethnically diverse community-based cohort: an HABS-HD study
(2025) Alzheimer’s and Dementia: Translational Research and Clinical Interventions, 11 (1), art. no. e70045, .
Petersen, M.E.a b , Zhang, F.a b , Hall, J.a b , Brock, C.a , Rissman, R.A.c , Como, T.a , Julovich, D.a , Mapstone, M.d , Ances, B.M.e , Meeker, K.a b , Palmer, R.f , Barber, R.a , Mason, D.b , Johnson, L.a , Yaffe, K.g h , Toga, A.W.i , Cohen, A.j , O’Bryant, S.E.a b , for the HABS-HD Study Teamk
a Institute for Translational Research, University of North Texas Health Science Center, Fort Worth, TX, United States
b Department of Family Medicine, University of North Texas Health Science Center, Fort Worth, TX, United States
c Keck School of Medicine of USC, San Diego, CA, United States
d Department of Neurology, University of California, Irvine School of Medicine, Irvine, CA, United States
e Department of Neurology, Washington University in St. Louis, St. Louis, MO, United States
f Department of Family Practice and Community Medicine, Joe R & Teresa Lozano Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX, United States
g Department of Psychiatry, Neurology, and Epidemiology and Biostatistics, University of California, San Francisco, CA, United States
h San Francisco VA Medical Center, San Francisco, CA, United States
i Laboratory of Neuro Imaging, USC Stevens Neuroimaging and Informatics Institute, Keck School of Medicine of USC, University of Southern California, Los Angeles, CA, United States
j Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, United States
Abstract
INTRODUCTION: Alzheimer’s disease (AD) biomarkers of Amyloid(A), Tau(T), and Neurodegeneration(N) have been increasingly studied to fill the gap in our understanding of racial and ethnic differences. This study aimed to examine the relationship between plasma AT(N) biomarkers and (1) AT(N) neuroimaging biomarkers, (2) demographics, (3) medical comorbidities, and (4) cognitive diagnosis. METHODS: Data were analyzed from n = 764 non-Hispanic Black (NHB), n = 1230 Hispanic, and n = 1232 non-Hispanic White (NHW) participants. Plasma AT(N) biomarkers were derived using single molecule array (SIMOA) technology on an HD-X imager and included amyloid beta (Aβ)42/40, total tau, ptau181, and neurofilament light chain (NfL). Clinical reads of positron emission tomography (PET) amyloid and tau positivity were used to examine the link between AT(N) plasma and neuroimaging biomarkers. Generalized linear models were conducted to examine the relationship between plasma AT(N) biomarkers and select demographic, diagnostic, and medical comorbidities (hypertension, diabetes, dyslipidemia, chronic kidney disease). RESULTS: Differences in the AT(N) biomarkers were found across racial/ethnic groups. Plasma Aβ42/40 was found to be associated with PET amyloid positivity only among NHW participants, while plasma NfL was found to correlate with Meta-ROI among NHB and Hispanic participants. Ptau181 was associated with PET amyloid positivity among NHB and NHW participants and well as PET tau positivity among the latter group and Hispanic participants. Diabetes was related to increased plasma AT(N) biomarkers among NHB and Hispanic participants. CKD was associated with increased AT(N) biomarkers for all race/ethnic groups with the exception of Aβ42/40. While Aβ42/40, total tau, ptau181, and NfL were found to be related to a dementia diagnosis among NHW participants, only ptau181 and NfL were found to be related to this same diagnostic category among NHB and Hispanic participants. DISCUSSION: Our findings indicate differential relationships between comorbidities (demographic, medical, diagnostic) across NHB, Hispanic, and NHW participants. This work expands our knowledge regarding the associations of plasma biomarkers to AD pathology in diverse populations. Highlights: Differences in AT(N) plasma biomarkers were found in a diverse community cohort. While plasma Aβ42/40 was associated with PET amyloid positivity among non-Hispanic white participants, this did not apply to non-Hispanic Black or Hispanic participants. Medical comorbidity of diabetes and chronic kidney disease was related to increased plasma AT(N) biomarkers among the ethnically diverse segment of the cohort. Plasma AT(N) biomarkers were more so related to a diagnosis of dementia for non-Hispanic white as compared to Hispanic or non-Hispanic Black participants. Across racial/ethnic groups, the plasma biomarkers of neurodegeneration (NfL) and ptau181 were related to a diagnosis of dementia. © 2025 The Author(s). Alzheimer’s & Dementia: Translational Research & Clinical Interventions published by Wiley Periodicals LLC on behalf of Alzheimer’s Association.
Author Keywords
AT(N); biomarkers; Black participants; community-based; Hispanic participants; plasma
Funding details
National Institute on AgingNIA
National Institutes of HealthNIHR01AG054073, R01AG058533, P41EB015922, U19AG078109
National Institutes of HealthNIH
Document Type: Article
Publication Stage: Final
Source: Scopus