Longitudinal Relationships of White Matter Hyperintensities and Alzheimer Disease Biomarkers Across the Adult Life Span
Open accessAbstract
Background and Objectives White matter hyperintensities (WMH) correlate with Alzheimer disease (AD) biomarkers cross-sectionally and modulate AD pathogenesis. Longitudinal changes have been reported for AD biomarkers, including concentrations of CSF β-amyloid (Aβ) 42, Aβ40, total tau and phosphorylated tau181, standardized uptake value ratio from the molecular imaging of cerebral fibrillar Aβ with PET using [ 11 C] Pittsburgh Compound-B, MRI-based hippocampal volume, and cortical thickness. Correlations between established AD biomarkers and the longitudinal change for WMH have not been fully evaluated, especially among cognitively normal individuals across the adult life span. Methods We jointly analyzed the longitudinal data of WMH volume and each of the established AD biomarkers and cognition from 371 cognitively normal individuals whose baseline age spanned from 19.6 to 88.20 years from 4 longitudinal studies of aging and AD. A 2-stage algorithm was applied to identify the inflection point of baseline age whereby older participants had an accelerated longitudinal change in WMH volume, in comparison with the younger participants. The longitudinal correlations between WMH volume and AD biomarkers were estimated from the bivariate linear mixed-effects models. Results A longitudinal increase in WMH volume was associated with a longitudinal increase in PET amyloid uptake and a decrease in MRI hippocampal volume, cortical thickness, and cognition. The inflection point of baseline age in WMH volume was identified at 60.46 (95% CI 56.43–64.49) years, with the annual increase for the older participants (83.12 [SE = 10.19] mm 3 per year) more than 13 times faster ( p < 0.0001) than that for the younger participants (6.35 [SE = 5.63] mm 3 per year). Accelerated rates of change among the older participants were similarly observed in almost all the AD biomarkers. Longitudinal correlations of WMH volume with MRI, PET amyloid biomarkers, and cognition seemed to be numerically stronger for the younger participants, but not significantly different from those for the older participants. Carrying APOE ε4 alleles did not alter the longitudinal correlations between WMH and AD biomarkers. Discussion Longitudinal increases in WMH volume started to accelerate around a baseline age of 60.46 years and correlated with the longitudinal change in PET amyloid uptake, MRI structural outcomes, and cognition.
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Only a few studies reported faster longitudinal WMH growth in individuals with higher baseline Aβ deposition.
“Only a few studies reported faster longitudinal WMH growth in individuals with higher baseline Aβ deposition. 35 , 61 , 62 , 63”
From White matter hyperintensity modulates the amyloid‐tau‐cognition association and anti‐amyloid treatment efficacy in asymptomatic older adults (2025) · cites this paper as [35]
The Results and the ‘Longitudinal Correlations Between WMH Volume and AD Biomarkers’ section report that faster WMH growth was associated with faster increases in PET amyloid uptake. They do not show that higher *baseline* Aβ deposition predicted faster subsequent WMH growth. The Discussion says earlier longitudinal WMH studies had focused on structural changes and cognition, not this amyloid relationship; page numbers were not available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe longitudinal correlation between WMH and AD pathology is stronger in younger participants, suggesting a potential age-dependent effect of amyloid on WMH.
“As reported in Luo et al., 35 the longitudinal correlation between WMH and AD pathology was stronger in younger participants, suggesting a potential age‐dependent effect of amyloid on WMH.”
From White matter hyperintensity modulates the amyloid‐tau‐cognition association and anti‐amyloid treatment efficacy in asymptomatic older adults (2025) · cites this paper as [35]
The Results say that longitudinal correlations between WMH and PET amyloid biomarkers appeared numerically stronger in younger participants, but the age-group differences were not statistically significant. The Discussion adds that correlations between WMH and amyloid biomarkers were not significant within the younger group; it does not establish an age-dependent effect of amyloid on WMH. Page numbers are unavailable in our copy. (LLM, conf=0.88)
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- nar series, Grand Rds, NY. A.M. Fagan has consulted for Bio- gen, Centene, Fujirebio, and Roche Diagnostics, is a member of the scientific advisory boards for Roche Diagnostics, Gen- entech, and AbbVie, and consults for Araclon/Grifols, Diadem, and DiamiR. T.L.S. Benzinger received research support from Avid Radiopharmaceuticals and participates in clinical trials sponsored by Avid Radiopharmaceuticals, Eli Lilly, and Hoffman-LaRoche and has received honoraria from Biogen, Eisai, and Genetech. R.J. Bateman has equity ownership in- terest in C2N Diagnostics and may receive income based on technology licensed or optioned by Washington University to C2N Diagnostics, receives income from C2N Diagnostics for serving on the scientific advisory board, received honoraria as a speaker/consultant/advisory board member from Amgen, Eisai, and Roche. B. Gordon participates in clinical trials sponsored by Avid Radio-pharmaceuticals (a wholly owned subsidiary of Eli Lilly), Eli Lilly, and Hoffman-LaRoche. G.S. Day is supported by the NIH/National Institute on Aging (K23AG064029), serves as a topic editor on dementia for DynaMed Plus (EBSCO Industries, Inc.), is a consultant for Parabon NanoLabs, is the clinical director for the Anti-NMDA Receptor Encephalitis Foundation (uncompensated), has provided record review and expert medical testimony on legal References
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- Authors
- Luo, J., Ma, Y., Agboola, F. J., Grant, E., Morris, J. C., McDade, E., Fagan, A. M., Benzinger, T. L. S., Hassenstab, J., Bateman, R. J., Perrin, R. J., Gordon, B. A., Goyal, M., Strain, J. F., Yakushev, I., Day, G. S., Xiong, C., & for Dominantly Inherited Alzheimer Network (DIAN)
- Affiliations
- From the Division of Public Health Sciences (J.L.), Department of Surgery, Siteman Cancer Center Biostatistics Core (J.L.), Division of Biostatistics (J.L., Y.M., F.J.A., E.G., C.X.), Knight Alzheimer Disease Research Center (Y.M., F.J.A., E.G., J.C.M., A.M.F., T.L.S.B., J.H., R.J.B., R.J.P., B.A.G., C.X.), Department of Neurology (J.C.M., E.M., A.M.F., J.H., R.J.B., R.J.P., M.G., J.F.S.), Department of Pathology and Immunology (J.C.M., R.J.P.), and Department of Radiology (T.L.S.B., B.A.G., M.G.),...
- ORCID
- Venue
- Neurology
- Published
- 2023-07-11
- Volume
- 101
- Issue
- 2
- Pages
- e164-e177
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC10351551
- OpenAlex
- W4377012437
- Cited by
- 35
- References
- 51
- Citations by year
- 2026: 12 · 2025: 15 · 2024: 6 · 2023: 2
- FWCI
- 7.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Funders
- Fondation Brain Canada
- Japan Agency for Medical Research and Development
- Korea Health Industry Development Institute
- Deutsches Zentrum für Neurodegenerative Erkrankungen
- Fleni
- National Institutes of Health (1s10od025214-01, UL1TR002345)
- Canadian Institutes of Health Research
- Charles F. and Joanne Knight Alzheimer Disease Research Center, Washington University in St. Louis
- Instituto de Salud Carlos III
- National Institute on Aging (U01AG057195, R01AG067505, UF1AG032438, R01AG054567, P50AG005681, P01AG003991, K23AG064029, U19AG032438, RF1AG053550, R01AG025350, P30AG066444, P01AG026276)
- National Institute of Neurological Disorders and Stroke (P30NS098577)
- National Institute of Biomedical Imaging and Bioengineering (R01EB009352)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- white matter hyperintensities, Alzheimer's disease biomarkers, longitudinal change, aging, amyloid PET, Pittsburgh compound B, hippocampal volume, cortical thickness, CSF tau, APOE ε4, cognitively normal older adults, cognitive decline, brain aging, amyloid accumulation, tau accumulation, cerebral small vessel disease
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Humans, Longevity, Longitudinal Studies, Magnetic Resonance Imaging, Middle Aged, Biomarkers, Amyloid beta-Peptides, tau Proteins, Positron-Emission Tomography, Young Adult, Cognitive Dysfunction, White Matter
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