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Cited by 60Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsDown syndrome and intellectual disability research

Characterizing the emergence of amyloid and tau burden in Down syndrome

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Zammit, Matthew D., Betthauser, Tobey J., McVea, Andrew K., Laymon, Charles M., Tudorascu, Dana L., Johnson, Sterling C., Hartley, Sigan L., Converse, Alexander K. +10 more·2024·Alzheimer's & Dementia
DOI 10.1002/alz.13444PMC PMC10843570
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Abstract

INTRODUCTION: Almost all individuals with Down syndrome (DS) will develop neuropathological features of Alzheimer's disease (AD). Understanding AD biomarker trajectories is necessary for DS‐specific clinical interventions and interpretation of drug‐related changes in the disease trajectory. METHODS: A total of 177 adults with DS from the Alzheimer's Biomarker Consortium‐Down Syndrome (ABC‐DS) underwent positron emission tomography (PET) and MR imaging. Amyloid‐beta (Aβ) trajectories were modeled to provide individual‐level estimates of Aβ‐positive (A+) chronicity, which were compared against longitudinal tau change. RESULTS: Elevated tau was observed in all NFT regions following A+ and longitudinal tau increased with respect to A+ chronicity. Tau increases in NFT regions I‐III was observed 0–2.5 years following A+. Nearly all A+ individuals had tau increases in the medial temporal lobe. DISCUSSION: These findings highlight the rapid accumulation of amyloid and early onset of tau relative to amyloid in DS and provide a strategy for temporally characterizing AD neuropathology progression that is specific to the DS population and independent of chronological age. Highlights: Longitudinal amyloid trajectories reveal rapid Aβ accumulation in Down syndrome NFT stage tau was strongly associated with A+ chronicity Early longitudinal tau increases were observed 2.5–5 years after reaching A+

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  • Recent natural history studies have highlighted evidence of accelerated AD progression in people who have DSAD, including a more rapid development of tau spread as measured by positron emission tomography and plasma phospho-tau217, and enhanced rates of cortical thinning, after normalising for amyloid-β accumulation.

    “Recent natural history studies comparing the development of AD in the general population and DSAD have highlighted evidence of accelerated AD progression in people who have DSAD. This includes a more rapid development of tau spread as measured by positron emission tomography and plasma phospho-tau217 [60, 68, 72], and enhanced rates of cortical thinning [37], after normalising for amyloid-β accum”

    From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [72]

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  • In DSAD, tau pathology develops faster in relation to amyloid-β than in AD in the general population.

    “These include a faster development of tau pathology in relation to amyloid-β [72]”

    From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [72]

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Authors
Zammit, M. D., Betthauser, T. J., McVea, A. K., Laymon, C. M., Tudorascu, D. L., Johnson, S. C., Hartley, S. L., Converse, A. K., Minhas, D. S., Zaman, S. H., Ances, B. M., Stone, C. K., Mathis, C. A., Cohen, A. D., Klunk, W. E., Handen, B. L., Christian, B. T., & the Alzheimer's Biomarker Consortium – Down Syndrome
Affiliations
  • University of Wisconsin–Madison (US)
  • University of Pittsburgh (US)
  • University of Cambridge (GB)
  • Washington University in St. Louis (US)
Corresponding author
Zammit, Matthew D.
ORCID
Venue
Alzheimer's & Dementia
Publisher
Wiley
Published
2023-08-29
Volume
20
Issue
1
Pages
388-398
ISSN
  • 1552-5260 (ISSN-L)
  • 1552-5279
DOI
10.1002/alz.13444
PMC
PMC10843570
OpenAlex
W4386253945
Cited by
60
References
65
Citations by year
2026: 19 · 2025: 28 · 2024: 13
FWCI
12.08
Type
journal article
Language
en
Open access
Licence
Locations
  • Alzheimer s & Dementia (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Apollo (University of Cambridge) (submittedVersion, cc-by)
Funders
  • National Institute for Health and Care Research
  • Department of Health and Social Care
  • National Institutes of Health (UL1TR001414, AG062421, HD105353, AG005133, AG005681, AG066519, HD090256, HD087011, AG008702, UL1TR001873, UL1TR001857, UL1TR002373, UL1TR002345)
  • NIHR Cambridge Biomedical Research Centre
  • National Institute on Aging (P50AG005133, U01AG051406, U01AG051412, P50AG008702, P50AG005681, P30AG066462, U19AG068054, P30AG066444, P30AG062715, U24AG021886, P30AG062421, P30AG066519)
  • National Institute of Child Health and Human Development (HD105353, HD090256, HD087011)
  • National Center for Advancing Translational Sciences (TR001873, TR002345, TR001857, TR001414)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD105353, U54HD090256, U54HD087011, HD087011, HD090256, P50HD105353)
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 › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
Keywords
Down syndrome, Alzheimer's disease
MeSH terms
Adult, Alzheimer Disease, Amyloid, Down Syndrome, Humans, Biomarkers, Amyloid beta-Peptides, tau Proteins, Positron-Emission Tomography

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