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Amyloid β-protein (Aβ)-containing astrocytes are located preferentially near N-terminal-truncated Aβ deposits in the human entorhinal cortex
Abstract
The deposition of the amyloid beta-protein (Abeta) is a pathological hallmark of Alzheimer's disease (AD). Abeta is a peptide consisting of 39-43 amino acids and is derived by beta- and gamma-secretase cleavage from the Abeta protein precursor (AbetaPP). An N-terminal-truncated form of Abeta can occur following alpha- and gamma-secretase cleavage of AbetaPP. Fleecy amyloid is a recently identified distinct type of Abeta deposits occurring in the internal layers (pri-alpha, pri-beta and pri-gamma) of the human entorhinal cortex. Fleecy amyloid consists exclusively of N-terminal-truncated Abeta and is a transient form of Abeta deposits, which disappears in late-stage beta-amyloidosis. In this study, the entorhinal cortex of 15 cases with AD-related pathology was used to examine astrocytes in the vicinity of N-terminal-truncated Abeta in fleecy amyloid of the layers pri-alpha, pri-beta, and pri-gamma in comparison to astrocytes in the vicinity of full-length Abeta in layers pre-beta and pre-gamma. Immunohistochemistry was performed with antibodies directed against AbetaPP, Abeta40, Abeta42, APbeta17-24, Abeta1-17 and Abeta8-17 as well as by double-labeling with antibodies directed against Abeta17-24, Abeta42, and glial fibrillary acid protein (GFAP). A large number of GFAP-positive astrocytes containing N-terminal-truncated Abeta fragments appeared in the vicinity of N-terminal-truncated Abeta, whereas Abeta-containing astrocytes were rarely seen in the vicinity of full-length A…
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“and Aβ has been observed in vesicles within astrocytes (57, 58).”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [58]
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Metadata
- Authors
- Thal, D. R., Schultz, C., Dehghani, F., Yamaguchi, H., Braak, H., & Braak, E.
- Affiliations
- Goethe University Frankfurt (DE)
- Gunma University (JP)
- Venue
- Acta Neuropathologica
- Published
- 2000-12-18
- Volume
- 100
- Issue
- 6
- Pages
- 608-617
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- OpenAlex
- W2087697089
- Cited by
- 136
- References
- 32
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 4 · 2023: 16 · 2022: 6 · 2021: 12 · 2020: 9 · 2019: 1 · 2018: 5 · 2017: 11 · 2016: 9 · 2015: 5 · 2014: 7 · 2013: 3 · 2012: 5
- FWCI
- 0.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Bundesministerium für Bildung und Forschung
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- amyloid-beta, entorhinal cortex, astrocytes, Alzheimer's disease, amyloid precursor protein, amyloid clearance, extracellular amyloid deposition, gamma-secretase, beta-secretase, glial fibrillary acidic protein
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Astrocytes, Female, Humans, Male, Middle Aged, Peptide Fragments, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Protein Structure, Tertiary, Entorhinal Cortex, Plaque, Amyloid
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