Extracellular vesicles from amyloid-β exposed cell cultures induce severe dysfunction in cortical neurons
Open accessAbstract
Alzheimer’s disease (AD) is characterized by a substantial loss of neurons and synapses throughout the brain. The exact mechanism behind the neurodegeneration is still unclear, but recent data suggests that spreading of amyloid-β (Aβ) pathology via extracellular vesicles (EVs) may contribute to disease progression. We have previously shown that an incomplete degradation of Aβ 42 protofibrils by astrocytes results in the release of EVs containing neurotoxic Aβ. Here, we describe the cellular mechanisms behind EV-associated neurotoxicity in detail. EVs were isolated from untreated and Aβ 42 protofibril exposed neuroglial co-cultures, consisting mainly of astrocytes. The EVs were added to cortical neurons for 2 or 4 days and the neurodegenerative processes were followed with immunocytochemistry, time-lapse imaging and transmission electron microscopy (TEM). Addition of EVs from Aβ 42 protofibril exposed co-cultures resulted in synaptic loss, severe mitochondrial impairment and apoptosis. TEM analysis demonstrated that the EVs induced axonal swelling and vacuolization of the neuronal cell bodies. Interestingly, EV exposed neurons also displayed pathological lamellar bodies of cholesterol deposits in lysosomal compartments. Taken together, our data show that the secretion of EVs from Aβ exposed cells induces neuronal dysfunction in several ways, indicating a central role for EVs in the progression of Aβ-induced pathology.
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The concentrations of αSYN-F and Aβ-F used were selected based on previous studies.
“The concentrations were selected based on our previous studies [11, 12, 23, 28, 29].”
From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [28]
The Materials and methods sections report a 0.1 µM Aβ42 protofibril exposure and say the protofibrils were prepared using a previously established protocol (page not available in our copy). This supports a connection to prior Aβ work, but the paper does not say that the exposure concentration was selected on that basis and does not address αSYN-F concentrations. (LLM, conf=0.78)
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Yakovlev, E. V., Simkin, I. V., Shirokova, A. A., Kolotyeva, N. A., Novikova, S. V., Nasyrov, A. D., Denisenko, I. R., Gursky, K. D., Shishkov, I. N., Narzaeva, D. E., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-59773-2 · Cited by 8 · see citing works
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Self-citationChiarini, A., Armato, U., Gui, L., Yin, M., Chang, S., & Prà, I. D. (2024) · Brain Research · doi:10.1016/j.brainres.2024.149283 · Cited by 7 · see citing works
Potential Roles of α-amylase in Alzheimer’s Disease: Biomarker and Drug Target
Chen, W. N., Tang, K. S., & Yeong, K. Y. (2021) · Current Neuropharmacology · doi:10.2174/1570159x20666211223124715 · Cited by 7 · see citing works
Zombosomes are anucleated cell couriers that spread α-synuclein pathology
Dakhel, A., Beretta, C., Mothes, T., Hakhverdyan, S., Michno, W., Rostami, J., & Erlandsson, A. (2026) · Cell Reports · doi:10.1016/j.celrep.2025.116831 · Cited by 6 · see citing works
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Tau processing and tau-mediated inflammation differ in human APOEε2 and APOEε4 astrocytes
Mothes, T., Konstantinidis, E., Eltom, K., Dakhel, A., Rostami, J., & Erlandsson, A. (2024) · iScience · doi:10.1016/j.isci.2024.111163 · Cited by 5 · see citing works
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Amyloid‐Related Imaging Abnormality (ARIA) Beyond the APOE‐ε4 Allele
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Self-citationZyśk, M., Beretta, C., Naia, L., Dakhel, A., Påvénius, L., Brismar, H., Lindskog, M., Ankarcrona, M., & Erlandsson, A. (2023) · Figshare · doi:10.6084/m9.figshare.22610228
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Self-citationMothes, T., Portal, B., Konstantinidis, E., Eltom, K., Libard, S., Streubel-Gallasch, L., Ingelsson, M., Rostami, J., Lindskog, M., & Erlandsson, A. (2024) · Figshare · doi:10.6084/m9.figshare.26598038
Self-citationMothes, T., Portal, B., Konstantinidis, E., Eltom, K., Libard, S., Streubel-Gallasch, L., Ingelsson, M., Rostami, J., Lindskog, M., & Erlandsson, A. (2024) · Figshare · doi:10.6084/m9.figshare.26598029
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Self-citationClarkson, B. D. S., Grund, E. M., David, K., Johnson, R. K., & Howe, C. L. (2022) · Figshare · doi:10.6084/m9.figshare.21366140
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Extracellular vesicles in Alzheimer’s disease: New perspectives on diagnosis and therapy
Klepe, A., Mi, J., Neuhaus, W., & Burek, M. (2026) · International review of neurobiology · doi:10.1016/bs.irn.2026.08.024
- Authors
- Beretta, C., Nikitidou, E., Streubel-Gallasch, L., Ingelsson, M., Sehlin, D., & Erlandsson, A.
- Affiliations
- Uppsala University (SE)
- Corresponding author
- Erlandsson, Anna
- Venue
- Scientific Reports
- Published
- 2020-11-12
- Volume
- 10
- Issue
- 1
- Pages
- 19656-19656
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC7661699
- OpenAlex
- W3099373101
- Cited by
- 71
- References
- 53
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 26 · 2023: 20 · 2022: 8 · 2021: 7
- FWCI
- 5.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- KTH Publication Database DiVA (KTH Royal Institute of Technology) (submittedVersion, other-oa)
- Funders
- Vetenskapsrådet (2018-02659)
- Åhlén-stiftelsen (mC17 h18)
- Stiftelsen Olle Engkvist Byggmästare (191-0410)
- Torsten Söderbergs Stiftelse (M60/18)
- Hjärnfonden (FO2018-0153)
- Alzheimerfonden (AF-930515)
- Gun och Bertil Stohnes Stiftelse
- Stiftelsen för Gamla Tjänarinnor
- Uppsala Berzelii Technology Centre for Neurodiagnostics
- Uppsala University
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- extracellular vesicles, amyloid-beta, Alzheimer's disease, astrocytes, cortical neurons, neurotoxicity, synaptic loss, mitochondrial dysfunction, apoptosis, axonal swellings, neurodegeneration
- MeSH terms
- Extracellular Vesicles, Alzheimer Disease, Animals, Astrocytes, Cells, Cultured, Cerebral Cortex, Mice, Inbred C57BL, Neurons, Amyloid beta-Peptides, Coculture Techniques, Microscopy, Electron, Transmission, Mice
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