Emergence of distinct and heterogeneous strains of amyloid beta with advanced Alzheimer’s disease pathology in Down syndrome
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Abstract
Amyloid beta (Aβ) is thought to play a critical role in the pathogenesis of Alzheimer’s disease (AD). Prion-like Aβ polymorphs, or “strains”, can have varying pathogenicity and may underlie the phenotypic heterogeneity of the disease. In order to develop effective AD therapies, it is critical to identify the strains of Aβ that might arise prior to the onset of clinical symptoms and understand how they may change with progressing disease. Down syndrome (DS), as the most common genetic cause of AD, presents promising opportunities to compare such features between early and advanced AD. In this work, we evaluate the neuropathology and Aβ strain profile in the post-mortem brain tissues of 210 DS, AD, and control individuals. We assayed the levels of various Aβ and tau species and used conformation-sensitive fluorescent probes to detect differences in Aβ strains among individuals and populations. We found that these cohorts have some common but also some distinct strains from one another, with the most heterogeneous populations of Aβ emerging in subjects with high levels of AD pathology. The emergence of distinct strains in DS at these later stages of disease suggests that the confluence of aging, pathology, and other DS-linked factors may favor conditions that generate strains that are unique from sporadic AD.
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α-synuclein and Aβ oligomers exhibit distinct strains that influence disease phenotypes.
“Like tau, α‐synuclein and Aβ oligomers also exhibit distinct strains that influence disease phenotypes.”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [170]
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- Authors
- Maxwell, A. M., Yuan, P., Rivera, B. M., Schaaf, W., Mladinov, M., Prasher, V. P., Robinson, A. C., DeGrado, W. F., & Condello, C.
- Affiliations
- University of California, San Francisco (US)
- San Francisco State University (US)
- Liverpool John Moores University (GB)
- University of Manchester (GB)
- Corresponding author
- Condello, Carlo
- ORCID
- Venue
- Acta Neuropathologica Communications
- Published
- 2021-12
- Volume
- 9
- Issue
- 1
- Pages
- 201-201
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC8711167
- OpenAlex
- W4200501434
- Cited by
- 23
- References
- 75
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 8 · 2023: 6 · 2022: 4
- FWCI
- 2.83
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (RF1AG061874, P01AG002132)
- National Science Foundation (2034836)
- National Institutes of Health (GM064337)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Keywords
- amyloid-beta, Down syndrome, Alzheimer's disease, tau protein, neuropathology, phenotypic heterogeneity, aging, postmortem brain
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Down Syndrome, Female, Humans, Male, Middle Aged, Amyloid beta-Peptides, tau Proteins, Young Adult
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