Longitudinal amyloid and tau accumulation in autosomal dominant Alzheimer’s disease: findings from the Colombia-Boston (COLBOS) biomarker study
Open accessAbstract
Background: Neuroimaging studies of autosomal dominant Alzheimer’s disease (ADAD) enable characterization of the trajectories of cerebral amyloid-β (Aβ) and tau accumulation in the decades prior to clinical symptom onset. Longitudinal rates of regional tau accumulation measured with positron emission tomography (PET) and their relationship with other biomarker and cognitive changes remain to be fully characterized in ADAD. Methods: Fourteen ADAD mutation carriers (Presenilin-1 E280A) and 15 age-matched non-carriers from the Colombian kindred underwent 2–3 sessions of Aβ (11C-Pittsburgh compound B) and tau (18F-flortaucipir) PET, structural magnetic resonance imaging, and neuropsychological evaluation over a 2–4-year follow-up period. Annualized rates of change for imaging and cognitive variables were compared between carriers and non-carriers, and relationships among baseline measurements and rates of change were assessed within carriers. Results: Longitudinal measurements were consistent with a sequence of ADAD-related changes beginning with Aβ accumulation (16 years prior to expected symptom onset, EYO), followed by entorhinal cortex (EC) tau (9 EYO), neocortical tau (6 EYO), hippocampal atrophy (6 EYO), and cognitive decline (4 EYO). Rates of tau accumulation among carriers were most rapid in parietal neocortex (~ 9%/year). EC tau PET signal at baseline was a significant predictor of subsequent neocortical tau accumulation and cognitive decline within carriers. Conclusions: Our results are consistent with the sequence of biological changes in ADAD implied by cross-sectional studies and highlight the importance of EC tau as an early biomarker and a potential link between Aβ burden and neocortical tau accumulation in ADAD.
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Some cases in a large kindred carrying the PSEN1 E280A mutation have shown delayed onset, suggesting possible mechanisms of disease modulation.
“Nevertheless, some cases belonging to a large kindred carrying the presenilin-1 (PSEN1) E280A mutation have shown delayed onset, suggesting possible mechanisms of disease modulation [31, 32].”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [31]
The Background describes the large Colombian PSEN1 E280A kindred, and the Discussion reports one carrier who retained cognitive function into her seventies despite substantial amyloid burden. The Discussion also suggests that factors beyond amyloid may affect disease progression. Our copy supports an unusually delayed case, but does not establish the claim’s plural “some cases.” Pages are not available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredOur findings provide evidence supporting tau pathology as the main driver of cognitive decline in PSEN E280A ADAD.
“Our findings provide evidence supporting tau pathology as the main driver of cognitive decline in PSEN E280A ADAD, as suggested by other previous findings in this population [31, 32]”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [31]
The Results section reports that baseline tau measures predicted subsequent cognitive decline in PSEN1 E280A carriers. The Discussion says tau change was more closely associated with cognitive decline than amyloid change, but those associations were not statistically significant; the paper does not establish tau pathology as the main causal driver. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn individuals with low baseline WMH, the strong correlation between Aβ accumulation and p-Tau217 change suggests a rapid pathogenetic cross-talk and a temporal sequence of successive amyloid and tau phosphorylation in early pre-clinical stage.
“Individuals with low baseline WMH exhibited a strong correlation between Aβ accumulation and p‐Tau217 change, consistent with previous findings, 33 , 36 , 37 suggesting a rapid pathogenetic cross‐talk and a temporal sequence of successive amyloid and tau phosphorylation in this early pre‐clinical stage.”
From White matter hyperintensity modulates the amyloid‐tau‐cognition association and anti‐amyloid treatment efficacy in asymptomatic older adults (2025) · cites this paper as [36]
The Discussion (page unavailable) reports that Aβ PET changes preceded tau PET changes in PSEN1 mutation carriers, supporting the proposed temporal sequence. It does not examine low baseline WMH or p-Tau217 change. The Results section “Aβ rise precedes rapid neocortical tau increase in ADAD” (page unavailable) instead reports that contemporaneous Aβ and tau PET change rates were not correlated in those carriers, so it does not support the claimed strong correlation or rapid cross-talk. (LLM, conf=0.88)
Experimental — accuracy not yet measuredWe previously reported the impact of tau pathology as a disease onset modifier and disease progression marker in vivo in this ADAD population.
“We previously reported the impact of tau pathology as a disease onset modifier [32] and disease progression marker in vivo [31] in this ADAD population.”
From Distinct tau neuropathology and cellular profiles of an APOE3 Christchurch homozygote protected against autosomal dominant Alzheimer’s dementia (2022) · cites this paper as [31]
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The probabilistic model of Alzheimer disease: the amyloid hypothesis revised
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Sepulveda-Falla, D., Sanchez, J. S., Almeida, M. C., Boassa, D., Acosta-Uribe, J., Vila-Castelar, C., Ramirez-Gomez, L., Baena, A., Aguillon, D., Villalba-Moreno, N. D., et al. (2022) · Acta Neuropathologica · doi:10.1007/s00401-022-02467-8 · Cited by 92 · see citing works
“We previously reported the impact of tau pathology as a disease onset modifier [32] and disease progression marker in vivo [31] in this ADAD population.”
BackgroundResultInfluentialSelf-citationYoung, C. B., Winer, J. R., Younes, K., Cody, K. A., Betthauser, T. J., Johnson, S. C., Schultz, A., Sperling, R. A., Greicius, M. D., Cobos, I., et al. (2022) · JAMA Neurology · doi:10.1001/jamaneurol.2022.0676 · Cited by 79 · see citing works
Self-citationLin, Z., Hong, Y., Hu, Y., Xiao, Q., Peng, S., Wu, D., Guo, T., & Jiang, D. (2025) · Alzheimer's & Dementia · doi:10.1002/alz.70990 · Cited by 2 · see citing works
- Authors
- Sanchez, J. S., Hanseeuw, B. J., Lopera, F., Sperling, R. A., Baena, A., Bocanegra, Y., Aguillon, D., Guzmán-Vélez, E., Pardilla-Delgado, E., Ramirez-Gomez, L., Vila-Castelar, C., Martinez, J. E., Fox-Fuller, J. T., Ramos, C., Ochoa-Escudero, M., Alvarez, S., Jacobs, H. I. L., Schultz, A. P., Gatchel, J. R., Becker, J. A., Katz, S. R., Mayblyum, D. V., Price, J. C., Reiman, E. M., Johnson, K. A., & Quiroz, Y. T.
- Affiliations
- Harvard University (US)
- Universidad de Antioquia (CO)
- Brigham and Women's Hospital (US)
- Banner Alzheimer’s Institute (US)
- Corresponding author
- Quiroz, Yakeel T.
- ORCID
- Sanchez, Justin S.
- Hanseeuw, Bernard J.
- Lopera, Francisco
- Sperling, Reisa A.
- Baena, Ana
- Bocanegra, Yamile
- Aguillon, David
- Ramirez-Gomez, Liliana
- Martinez, Jairo E.
- Jacobs, Heidi I. L.
- Schultz, Aaron P.
- Gatchel, Jennifer R.
- Becker, J. Alex
- Katz, Samantha R.
- Price, Julie C.
- Reiman, Eric M.
- Johnson, Keith A.
- Quiroz, Yakeel T.
- Venue
- Alzheimer's Research & Therapy
- Published
- 2021-01-15
- Volume
- 13
- Issue
- 1
- Pages
- 27-27
- ISSN
- 1758-9193 (ISSN-L)
- PMC
- PMC7811244
- OpenAlex
- W3124610746
- Cited by
- 58
- References
- 62
- Citations by year
- 2026: 8 · 2025: 13 · 2024: 3 · 2023: 9 · 2022: 17 · 2021: 8
- FWCI
- 6.63
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Alzheimer s Research & Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repository University of Antioquia (University of Antioquia) (publishedVersion, cc-by)
- Research Publications (Maastricht University) (publishedVersion, cc-by)
- Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Repositorio Digital - Academia Colombiana de Ciencias Exactas, Fisicas y Naturales (submittedVersion, other-oa)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Funders
- NIH Office of the Director (DP5OD019833)
- National Institute on Aging (R01AG054671, R01AG062559, 1F31AG062158-01A1, AG058805-01, R01 AG031581, P30 AG19610, P01AG036694, P50AG005134, 2009-2020, and U19 AG10483, R01 AG027435, AG036694, R01 AG046396, R13 AG042201174210, and U01AG024904)
- Alzheimer's Association (AACF_16-440965)
- Massachusetts General Hospital ECOR (1200-228010 and 1200-228767)
- Departamento Administrativo de Ciencia, Tecnología e Innovación (111565741185)
- BrightFocus Foundation (ADRF A2016434F)
- Massachusetts General Hospital (Rappaport Fellowship)
- Banner Alzheimer’s Foundation
- NOMIS Foundation
- Josephine and John Marr Alzheimer's Research Fund
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- autosomal dominant Alzheimer's disease, presenilin-1 E280A mutation, amyloid-beta deposition, tau accumulation, longitudinal biomarker trajectories, hippocampal atrophy, cognitive decline, 11C-Pittsburgh compound B, 18F-flortaucipir, preclinical Alzheimer's disease, mutation carriers
- MeSH terms
- Alzheimer Disease, Boston, Colombia, Cross-Sectional Studies, Humans, Magnetic Resonance Imaging, Biomarkers, Amyloid beta-Peptides, tau Proteins, Positron-Emission Tomography
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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