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Cited by 267Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons

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Söllvander, Sofia, Nikitidou, Elisabeth, Brolin, Robin, Söderberg, Linda, Sehlin, Dag, Lannfelt, Lars, Erlandsson, Anna·2016·Molecular Neurodegeneration
DOI 10.1186/s13024-016-0098-zPMC PMC4865996
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Abstract

BACKGROUND: Despite the clear physical association between activated astrocytes and amyloid-β (Aβ) plaques, the importance of astrocytes and their therapeutic potential in Alzheimer's disease remain elusive. Soluble Aβ aggregates, such as protofibrils, have been suggested to be responsible for the widespread neuronal cell death in Alzheimer's disease, but the mechanisms behind this remain unclear. Moreover, ineffective degradation is of great interest when it comes to the development and progression of neurodegeneration. Based on our previous results that astrocytes are extremely slow in degrading phagocytosed material, we hypothesized that astrocytes may be an important player in these processes. Hence, the aim of this study was to clarify the role of astrocytes in clearance, spreading and neuronal toxicity of Aβ. RESULTS: To examine the role of astrocytes in Aβ pathology, we added Aβ protofibrils to a co-culture system of primary neurons and glia. Our data demonstrates that astrocytes rapidly engulf large amounts of Aβ protofibrils, but then store, rather than degrade the ingested material. The incomplete digestion results in a high intracellular load of toxic, partly N-terminally truncated Aβ and severe lysosomal dysfunction. Moreover, secretion of microvesicles containing N-terminally truncated Aβ, induce apoptosis of cortical neurons. CONCLUSIONS: Taken together, our results suggest that astrocytes play a central role in the progression of Alzheimer's disease, by accumulating and spreading toxic Aβ species.

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  • In the AD and PD brain, both astrocytes and microglia acquire reactive, inflammatory phenotypes and can effectively phagocytose aggregated proteins and cell debris, as well as secrete various cytokines and inflammatory mediators.

    “In the AD and PD brain, both astrocytes and microglia acquire reactive, inflammatory phenotypes and can effectively phagocytose aggregated proteins and cell debris, as well as secrete various cytokines and inflammatory mediators [8–13].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [12]

    The Background (page unavailable) describes reactive astrocytes and microglia around amyloid plaques in AD, says both secrete cytokines, and reports that astrocytes engulf dead cells and protein aggregates. It does not establish the same combined account for both cell types in PD brains; the Discussion also cautions that astrocytes degrade ingested aggregates slowly. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The αSYN and Aβ accumulation result in severe cellular stress, indicated by lysosomal and mitochondrial deficiencies.

    “The αSYN and Aβ accumulation result in severe cellular stress, indicated by lysosomal and mitochondrial deficiencies [11, 12, 23].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [12]

    The Background and Conclusion (pages unavailable in our copy) state that intracellular Aβ accumulation in astrocytes causes severe endosomal and lysosomal defects. The paper does not establish the sentence’s claims about αSYN accumulation or mitochondrial deficiencies. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Microglia and astrocytes are responsible for many inflammatory processes in affected brains, including phagocytosis of αSYN and Aβ aggregates, secretion of inflammatory mediators, and stimulation of the innate immune system.

    “Microglia and astrocytes are known to be responsible for many inflammatory processes in affected brains, including phagocytosis of αSYN and Aβ aggregates, secretion of inflammatory mediators, and stimulation of the innate immune system [8–12].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [12]

    The Background (page not provided) says astrocytes engulf Aβ and α-synuclein aggregates, and that astrocytes and microglia secrete cytokines and neurotoxic products around Aβ plaques. It does not establish phagocytosis of both aggregates by microglia or state that these cells stimulate the innate immune system. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Astrocytes easily degrade αSYN and Aβ monomers, while they accumulate larger oligomers and fibrils.

    “These observations are in line with our previous discoveries that astrocytes easily degrade αSYN and Aβ monomers, while they accumulate larger oligomers and fibrils [11, 12].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [12]

    The Results section reports that astrocytes did not accumulate Aβ40 monomers but retained Aβ42 protofibrils, degrading them only slowly. The Discussion interprets this as a contrast between monomers and aggregated Aβ. This paper does not establish the same pattern for αSYN or for mature fibrils; those parts of the sentence are not supported by this source. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Cultured astrocytes accumulate αSYN and Aβ aggregates but not the monomeric form of the proteins.

    “We have previously reported that cultured astrocytes accumulate αSYN and Aβ aggregates but not the monomeric form of the proteins [11, 12].”

    From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [12]

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References 84 · Cited by 267

Research works printed but not linked: 64

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Authors
Söllvander, S., Nikitidou, E., Brolin, R., Söderberg, L., Sehlin, D., Lannfelt, L., & Erlandsson, A.
Affiliations
  • Uppsala University (SE)
  • BioArctic Neuroscience (Sweden) (SE)
Corresponding author
Erlandsson, Anna
ORCID
Venue
Molecular Neurodegeneration
Publisher
Springer Science and Business Media LLC
Published
2016-05-12
Volume
11
Issue
1
Pages
38-38
ISSN
1750-1326 (ISSN-L)
DOI
10.1186/s13024-016-0098-z
PMC
PMC4865996
OpenAlex
W2237384747
Cited by
267
References
84
Citations by year
2026: 25 · 2025: 29 · 2024: 37 · 2023: 40 · 2022: 25 · 2021: 34 · 2020: 25 · 2019: 12 · 2018: 17 · 2017: 21 · 2016: 1
FWCI
13.69
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Molecular Neurodegeneration (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Uppsala University Publications (Uppsala University) (submittedVersion, other-oa)
Funders
  • Vetenskapsrådet (#2012-2172)
  • Alzheimer's Foundation
  • Åhlén foundation
  • Stohnes Foundation
  • Magnus Bergvalls Foundation
  • Uppsala Berzelii Centre
Topics
  • Health Sciences › Medicine › Physiology › 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, astrocytes, Alzheimer's disease, amyloid protofibrils, lysosomal dysfunction, microvesicles, neuronal apoptosis, amyloid clearance, phagocytosis, neurodegeneration
MeSH terms
Alzheimer Disease, Animals, Astrocytes, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Immunohistochemistry, Mice, Inbred C57BL, Neurons, Endosomes, Blotting, Western, Amyloid beta-Peptides, Apoptosis, Coculture Techniques, Microscopy, Electron, Transmission, Mice, Cell-Derived Microparticles, Time-Lapse Imaging

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