Impact of increased APP gene dose in Down syndrome and the Dp16 mouse model
Open accessAbstract
Introduction: People with Down syndrome (DS) are predisposed to Alzheimer's disease (AD). The amyloid hypothesis informs studies of AD. In AD‐DS, but not sporadic AD, increased APP copy number is necessary, defining the APP gene dose hypothesis. Which amyloid precursor protein (APP) products contribute needs to be determined. Methods: Brain levels of full‐length protein (fl‐hAPP), C‐terminal fragments (hCTFs), and amyloid beta (Aβ) peptides were measured in DS, AD‐DS, non‐demented controls (ND), and sporadic AD cases. The APP gene‐dose hypothesis was evaluated in the Dp16 model. Results: DS and AD‐DS differed from ND and AD for all APP products. In AD‐DS, Aβ42 and Aβ40 levels exceeded AD. APP products were increased in the Dp16 model; increased APP gene dose was necessary for loss of vulnerable neurons, tau pathology, and activation of astrocytes and microglia. Discussion: Increases in APP products other than Aβ distinguished AD‐DS from AD. Deciphering AD‐DS pathogenesis necessitates deciphering which APP products contribute and how.
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Previous reports have shown increased abundance of APP, S100B, and SYNJ1 in the frontal cortex and CSTB in the temporal cortex of people with DSAD.
“These findings were consistent with previous reports of increased abundance of APP (amyloid precursor protein), S100B (S100 calcium-binding protein B), and SYNJ1 (synaptojanin-1) in the frontal cortex and CSTB (cystatin-B) in the temporal cortex of people with DSAD [45, 58, 71].”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [58]
The Preliminary Findings (page unavailable) report increased full-length APP in frozen frontal-cortex samples from people with AD-DS compared with non-demented controls. The cited paper does not report the claimed increases in S100B or SYNJ1 in frontal cortex or CSTB in temporal cortex. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn trisomy 21 (Down syndrome), the additional copy of chromosome 21 leads to APP gene overexpression, causing excessive Aβ accumulation and near-universal development of amyloid plaques and Alzheimer-type dementia by the fifth decade of life.
“Interestingly, in trisomy 21 (Down syndrome), the additional copy of chromosome 21 leads to APP gene overexpression, causing excessive Aβ accumulation and near-universal development of amyloid plaques and Alzheimer-type dementia by the fifth decade of life [150, 151].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [151]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAPP abundance was increased in the DSAD frontal cortex.
“Consistent with our proteomic analysis and a previous report [58], we found that APP abundance was increased in the DSAD frontal cortex (Fig. 4d, e).”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [58]
The increased APP-CTF-α in DSAD is likely the result of the additional copy of APP in individuals with DS.
“This is likely the result of the additional copy of APP in individuals with DS and is consistent with a previous report [58].”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [58]
Raised APP abundance in the DSAD cases is driven by the additional copy of APP on Hsa21.
“Importantly here, we know that raised APP abundance in our DSAD cases is driven by the additional copy of APP on Hsa21, as indicated by both human-genetics studies and preclinical modelling [12, 54, 58].”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [58]
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Cell models for Down syndrome-Alzheimer’s disease research
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Alzheimer's polygenic risk scores are associated with cognitive phenotypes in Down syndrome
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Self-citationThe history of Down syndrome–associated Alzheimer's disease; past, present, and future
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“These findings were consistent with previous reports of increased abundance of APP (amyloid precursor protein), S100B (S100 calcium-binding protein B), and SYNJ1 (synapto-janin-1) in the frontal cortex and CSTB (cystatin-B) in the temporal cortex of people with DSAD [45, 58, 71].”
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Chromosomal and cellular therapeutic approaches for Down syndrome: A research update
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Impact of Cre/LoxP-Mediated Chromosome Engineering Technology on Down Syndrome Research
Xing, Z., Douglas, A., Pao, A., Glass, T. J., Connor, N. P., & Yu, Y. E. (2025) · Springer eBooks · doi:10.1007/978-3-031-78611-2_2
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Jiang, X., Liu, C., Xing, Z., Li, Y., Douglas, A., Gao, L., Pao, A., Silverman, J., & Yu, E. Y. (2026) · G3 Genes Genomes Genetics · doi:10.1093/g3journal/jkag173
- Authors
- Sawa, M., Overk, C., Becker, A., Derse, D., Albay, R., Weldy, K., Salehi, A., Beach, T. G., Doran, E., Head, E., Yu, Y. E., & Mobley, W. C.
- Affiliations
- University of California San Diego (US)
- Stanford Medicine (US)
- Banner Sun Health Research Institute (US)
- University of California, Irvine (US)
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Mobley, William C
- ORCID
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2021-11-10
- Volume
- 18
- Issue
- 6
- Pages
- 1203-1234
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC9085977
- OpenAlex
- W3211991404
- Cited by
- 54
- References
- 178
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 10 · 2023: 17 · 2022: 4
- FWCI
- 6.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Alzheimer s & Dementia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (R01AG055523, R01AG061151 10 (WM), R01NS066072 (YEY))
- National Institute on Aging (U19AG068054, P30AG066519 (EH))
- Topics
- 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
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Down syndrome, Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Down Syndrome, Humans, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Gene Dosage, Mice
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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.
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