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Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation
Open accessAbstract
Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein. Because the neuropathological phenotype in older DS subjects closely resembles that of AD, the examination of DS brains of increasing age provides a unique model of the progression of AD. Here, we characterized the deposition of several A beta peptides and apolipoprotein E in formalin-fixed brain sections from 29 DS subjects between 3 and 73 years old. Amyloid plaque number and the percentage of cortical area they occupied were quantified by computerized image analysis. A beta ending at amino acid 42 (A beta 42) was the earliest form of A beta deposited in DS cortex. It was observed in 7 of 16 young (3-30 years) subjects, with the earliest deposition occurring at age 12. A beta ending at residue 40 (A beta 40) was not detected until approximately age 30, a time when degenerating neurites around A beta immunoreactive (IR) plaques were first observed, and the frequency of A beta 40 IR plaques then rose with age. Even in old (51-73 years) DS subjects, A beta 42 IR plaques were always more abundant than A beta 40 IR plaques. A beta peptides starting at aspartate 1 or pyroglutamate 3 were detected in small subsets of compacted, neuritic plaques beginning around age 30 and rose with age, the latter species always exceeding the former. Thus, the N-termini of the A beta 42 peptides abundantly deposited in very young DS subjects remain unknown. Apo E was detectable in a small subset of A beta 42 IR plaques beginning at age 12 and rose steadily with age; it clearly followed the deposition of A beta. Our analysis of very young DS brains suggests that amyloid plaque formation begins with A beta 42-ending peptides, and the number and percentage of cortical area of A beta 42 plaques increase very little with advancing age, while other heterogeneous A beta species and Apo E progressively accrue onto plaques containing A beta 42.
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“As previously reported [39], APOE staining resembles the pattern of amyloid-β plaque pathology in DSAD and EOAD cases, with minimal staining in HA cases (Supplementary Fig. 9).”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [39]
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“Consistent with the known sequestration of APOE within amyloid-β plaques [39], which we also observe in this study, the differences in amyloid-β plaques in DSAD that affect the sequestration of APOE may contribute to the differences in APOE abundance we observe.”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [39]
In the citing paper
“Down syndrome (DS) patients with trisomy-21 having extra copy of APP gene develop typical Alzheimer’s neuropathology including amyloid plaques and neurofibrillary tangles.35–37”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [37]
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“the earliest Aβ42 in plaques appears to be N-truncated [98].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [98]
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“N-terminal Aβ1-x/βCTF-specific antibodies also fail to label N-truncated Aβ42 peptides that appear to be particularly important in AD [60, 98, 157, 158, 206].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [98]
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- Evans, K. C., Berger, E. P., Cho, C.-G., Weisgraber, K. H., & Lansbury, P. T., Jr. (1995) Apolipoprotein E is a kinetic but not a thermody- namic inhibitor of amyloid formation: Implications for the patho- genesis and treatment of Alzheimer disease. Proc. Natl. Acad. Sci. USA 92, 763-767.
- Haass, C., Koo, E. H., Teplow, D. B., & Selkoe, D. J. (1994b) Polarized secretion of b-amyloid precursor protein and amyloid b-peptide in MDCK cells. Proc. Natl. Acad. Sci. USA 91, 1564-1568.
- Hyman, B. T., West, H. L., Rebeck, G. W., Buldyrev, S. V., Mantegna, R. N., Ukleja, M., Havlin, S., & Stanley, H. E. (1995) Quantitative analysis of senile plaques in Alzheimer's disease: Observation of log-normal size distribution and molecular epidemiology of differ- ences associated with apolipoprotein E genotype and trisomy 21 (Down syndrome). Proc. Natl. Acad. Sci. USA 92, 3586-3590.
- Malamud, N. (1972) Neuropathology of Organic Brain Syndromes Associated with Aging. Aging and the Brain: Advances in Behavioral Biology, Vol. 3, pp. 63-87. Plenum, New York.
- Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDon- ald, B. L., & Beyreuther, K. (1985) Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc. Natl. Acad. Sci. USA 82, 4245-4249.
- Schmechel, D. E., Saunders, A. M., Strittmatter, W. J., Crain, B. J., Hulette, C. M., Joo, S. H., Pericak-Vance, M. A., Goldgaber, D., & Roses, A. D. (1993) Increased amyloid b-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. Proc. Natl. Acad. Sci. USA 90, 9649- 9653.
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Metadata
- Authors
- Lemere, C. A., Blusztajn, J. K., Yamaguchi, H., Wisniewski, T., Saido, T. C., & Selkoe, D. J.
- Affiliations
- Boston University (US)
- Gunma University (JP)
- Tokyo Metropolitan Institute of Medical Science (JP)
- Brigham and Women's Hospital (US)
- Corresponding author
- Selkoe, D.J.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 1996-02
- Volume
- 3
- Issue
- 1
- Pages
- 16-32
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W1985323612
- Cited by
- 584
- References
- 0
- Citations by year
- 2026: 8 · 2025: 17 · 2024: 24 · 2023: 12 · 2022: 17 · 2021: 27 · 2020: 20 · 2019: 18 · 2018: 18 · 2017: 18 · 2016: 17 · 2015: 21 · 2014: 22 · 2013: 15 · 2012: 17
- FWCI
- 14.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Foundation for Neurologic Diseases
- National Institutes of Health
- National Institute on Aging (AG 12749, AG-06173, R01AG012749)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, amyloid-beta, amyloid plaques, apolipoprotein E, amyloid-beta 42, Aβ40, neuritic plaques, Alzheimer's disease, amyloid precursor protein, cortical amyloid deposition
- MeSH terms
- Adolescent, Adult, Aged, Aging, Alzheimer Disease, Apolipoproteins E, Child, Child, Preschool, Down Syndrome, Female, Humans, Immunoenzyme Techniques, Male, Middle Aged, Nerve Tissue Proteins, Peptide Fragments, Staining and Labeling, Temporal Lobe, Amyloid beta-Peptides, Neurites, Amyloid beta-Protein Precursor, Neurofibrillary Tangles
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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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