Cited by 237Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchPrion Diseases and Protein Misfolding

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Soluble Aβ Seeds Are Potent Inducers of Cerebral β-Amyloid Deposition

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Langer, Franziska, Eisele, Yvonne S., Fritschi, Sarah K., Staufenbiel, Matthias, Walker, Lary C., Jucker, Mathias·2011·The Journal of Neuroscience

DOI 10.1523/jneurosci.3088-11.2011PMC PMC3229270

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Abstract

Cerebral β-amyloidosis and associated pathologies can be exogenously induced by the intracerebral injection of small amounts of pathogenic Aβ-containing brain extract into young β-amyloid precursor protein (APP) transgenic mice. The probable β-amyloid-inducing factor in the brain extract has been identified as a species of aggregated Aβ that is generated in its most effective conformation or composition in vivo. Here we report that Aβ in the brain extract is more proteinase K (PK) resistant than is synthetic fibrillar Aβ, and that this PK-resistant fraction of the brain extract retains the capacity to induce β-amyloid deposition upon intracerebral injection in young, pre-depositing APP23 transgenic mice. After ultracentrifugation of the brain extract, <0.05% of the Aβ remained in the supernatant fraction, and these soluble Aβ species were largely PK sensitive. However, upon intracerebral injection, this soluble fraction accounted for up to 30% of the β-amyloid induction observed with the unfractionated extract. Fragmentation of the Aβ seeds by extended sonication increased the seeding capacity of the brain extract. In summary, these results suggest that multiple Aβ assemblies, with various PK sensitivities, are capable of inducing β-amyloid aggregation in vivo. The finding that small and soluble Aβ seeds are potent inducers of cerebral β-amyloidosis raises the possibility that such seeds may mediate the spread of β-amyloidosis in the brain. If they can be identified in vivo, soluble Aβ seeds in bodily fluids also could serve as early biomarkers for cerebral β-amyloidogenesis and eventually Alzheimer's disease.

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Self-citation

Authors: Langer, F., Eisele, Y. S., Fritschi, S. K., Staufenbiel, M., Walker, L. C., & Jucker, M.
Affiliations: Hertie Institute for Clinical Brain Research (DE)
German Center for Neurodegenerative Diseases (DE)
Novartis (Switzerland) (CH)
Emory University (US)
ORCID: Langer, Franziska
Eisele, Yvonne S.
Fritschi, Sarah K.
Walker, Lary C.
Jucker, Mathias
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2011-10-12
Volume: 31
Issue: 41
Pages: 14488-14495
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.3088-11.2011
PMC: PMC3229270
OpenAlex: W1991462232
Cited by: 237
References: 49
Citations by year: 2026: 5 · 2025: 7 · 2024: 6 · 2023: 8 · 2022: 8 · 2021: 29 · 2020: 12 · 2019: 15 · 2018: 19 · 2017: 16 · 2016: 24 · 2015: 20 · 2014: 29 · 2013: 19 · 2012: 14
FWCI: 14.84
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: public-domain
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 183 d)
Locations: Journal of Neuroscience (publishedVersion, public-domain)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
DZNE Pub (publishedVersion)
Funders: Bundesministerium für Bildung und Forschung (01GI0705)
National Institutes of Health (RR‐00165)
National Center for Research Resources (P51RR000165)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
Keywords: amyloid-beta aggregation, proteinase K resistance, APP23 transgenic mice, intracerebral injection, sonication, Alzheimer's disease, biomarkers
MeSH terms: Animals, Brain, Cerebral Cortex, Enzyme-Linked Immunosorbent Assay, Female, Male, Mice, Inbred C57BL, Mice, Transgenic, Peptide Fragments, Sonication, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Endopeptidase K, Mice

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Soluble Aβ Seeds Are Potent Inducers of Cerebral β-Amyloid Deposition

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