TY - JOUR
T1 - Socioeconomic Status Mediates Racial Differences Seen Using the AT(N) Framework
AU - Meeker, Karin L.
AU - Wisch, Julie K.
AU - Hudson, Darrell
AU - Coble, Dean
AU - Xiong, Chengjie
AU - Babulal, Ganesh M.
AU - Gordon, Brian A.
AU - Schindler, Suzanne E.
AU - Cruchaga, Carlos
AU - Flores, Shaney
AU - Dincer, Aylin
AU - Benzinger, Tammie L.
AU - Morris, John C.
AU - Ances, Beau M.
N1 - Funding Information:
This work was funded by the National Institute of Health (NIH) grants R01NR012907 (B.A.), R01NR012657 (B.A.), R01NR014449 (B.A.), P01AG00391 (J.C.M.), P01AG026276 (J.C.M.), and P01AG005681 (J.C.M.). This work was also supported by the generous support of Barnes‐Jewish Hospital, the Washington University Institute of Clinical and Translational Sciences Foundation (UL1 TR000448), the Hope Center for Neurological Disorders, the Paula and Rodger O. Riney Fund, the Daniel J. Brennan MD Fund, and the Fred Simmons and Olga Mohan Fund. The team thanks all participants involved in this study. Support for Florbetapir F18 (18F‐AV‐45) and Flortaucipir F18 (18F‐AV‐1451) was provided by Avid Radiopharmaceuticals, a wholly owned subsidiary of Eli Lilly.
Funding Information:
This work was funded by the National Institute of Health (NIH) grants R01NR012907 (B.A.), R01NR012657 (B.A.), R01NR014449 (B.A.), P01AG00391 (J.C.M.), P01AG026276 (J.C.M.), and P01AG005681 (J.C.M.). This work was also supported by the generous support of Barnes-Jewish Hospital, the Washington University Institute of Clinical and Translational Sciences Foundation (UL1 TR000448), the Hope Center for Neurological Disorders, the Paula and Rodger O. Riney Fund, the Daniel J. Brennan MD Fund, and the Fred Simmons and Olga Mohan Fund. The team thanks all participants involved in this study. Support for Florbetapir F18 (18F-AV-45) and Flortaucipir F18 (18F-AV-1451) was provided by Avid Radiopharmaceuticals, a wholly owned subsidiary of Eli Lilly.
Publisher Copyright:
© 2020 American Neurological Association
PY - 2021/2
Y1 - 2021/2
N2 - Objectives: African Americans are at greater risk for developing Alzheimer's disease (AD) dementia than non-Hispanic whites. In addition to biological considerations (eg, genetic influences and comorbid disorders), social and environmental factors may increase the risk of AD dementia. This paper (1) assesses neuroimaging biomarkers of amyloid (A), tau (T), and neurodegeneration (N) for potential racial differences and (2) considers mediating effects of socioeconomic status (SES) and measures of small vessel and cardiovascular disease on observed race differences. Methods: Imaging measures of AT(N) (amyloid and tau positron emission tomography [PET]) structural magnetic resonance imaging (MRI), and resting state functional connectivity (rs-fc) were collected from African American (n = 131) and white (n = 685) cognitively normal participants age 45 years and older. Measures of small vessel and cardiovascular disease (white matter hyperintensities [WMHs] on MRI, blood pressure, and body mass index [BMI]) and area-based SES were included in mediation analyses. Results: Compared to white participants, African American participants had greater neurodegeneration, as measured by decreased cortical volumes (Cohen's f2 = 0.05, p < 0.001). SES mediated the relationship between race and cortical volumes. There were no significant race effects for amyloid, tau, or rs-fc signature. Interpretation: Modifiable factors, such as differences in social contexts and resources, particularly area-level SES, may contribute to observed racial differences in AD. Future studies should emphasize collection of relevant psychosocial factors in addition to the development of intentional diversity and inclusion efforts to improve the racial/ethnic and socioeconomic representativeness of AD studies. ANN NEUROL 2021;89:254–265.
AB - Objectives: African Americans are at greater risk for developing Alzheimer's disease (AD) dementia than non-Hispanic whites. In addition to biological considerations (eg, genetic influences and comorbid disorders), social and environmental factors may increase the risk of AD dementia. This paper (1) assesses neuroimaging biomarkers of amyloid (A), tau (T), and neurodegeneration (N) for potential racial differences and (2) considers mediating effects of socioeconomic status (SES) and measures of small vessel and cardiovascular disease on observed race differences. Methods: Imaging measures of AT(N) (amyloid and tau positron emission tomography [PET]) structural magnetic resonance imaging (MRI), and resting state functional connectivity (rs-fc) were collected from African American (n = 131) and white (n = 685) cognitively normal participants age 45 years and older. Measures of small vessel and cardiovascular disease (white matter hyperintensities [WMHs] on MRI, blood pressure, and body mass index [BMI]) and area-based SES were included in mediation analyses. Results: Compared to white participants, African American participants had greater neurodegeneration, as measured by decreased cortical volumes (Cohen's f2 = 0.05, p < 0.001). SES mediated the relationship between race and cortical volumes. There were no significant race effects for amyloid, tau, or rs-fc signature. Interpretation: Modifiable factors, such as differences in social contexts and resources, particularly area-level SES, may contribute to observed racial differences in AD. Future studies should emphasize collection of relevant psychosocial factors in addition to the development of intentional diversity and inclusion efforts to improve the racial/ethnic and socioeconomic representativeness of AD studies. ANN NEUROL 2021;89:254–265.
UR - http://www.scopus.com/inward/record.url?scp=85096633987&partnerID=8YFLogxK
U2 - 10.1002/ana.25948
DO - 10.1002/ana.25948
M3 - Article
C2 - 33111990
AN - SCOPUS:85096633987
SN - 0364-5134
VL - 89
SP - 254
EP - 265
JO - Annals of neurology
JF - Annals of neurology
IS - 2
ER -