{"entity": "journal", "iuid": "87c60d901fe9446ba946cdcf24263d7b", "timestamp": "2026-08-23T09:24:48.534Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/Mol%20Cell%20Neurosci.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/Mol%20Cell%20Neurosci"}}, "title": "Mol Cell Neurosci", "issn": "1095-9327", "issn-l": null, "publications_count": 1, "publications": [{"entity": "publication", "iuid": "60c90f7000d84d6fbf556e99ca667b63", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/60c90f7000d84d6fbf556e99ca667b63.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/60c90f7000d84d6fbf556e99ca667b63"}}, "title": "Amyloid-\u03b2 deposits in human astrocytes contain truncated and highly resistant proteoforms.", "authors": [{"family": "Beretta", "given": "C", "initials": "C"}, {"family": "Svensson", "given": "E", "initials": "E"}, {"family": "Dakhel", "given": "A", "initials": "A"}, {"family": "Zy\u015bk", "given": "M", "initials": "M"}, {"family": "Hanrieder", "given": "J", "initials": "J"}, {"family": "Sehlin", "given": "D", "initials": "D"}, {"family": "Michno", "given": "W", "initials": "W"}, {"family": "Erlandsson", "given": "A", "initials": "A"}], "type": "journal article", "published": "2024-03-00", "journal": {"title": "Mol Cell Neurosci", "issn": "1095-9327", "volume": "128", "pages": "103916", "issn-l": null}, "abstract": "Alzheimer's disease (AD) is a neurodegenerative disorder that develops over decades. Glial cells, including astrocytes are tightly connected to the AD pathogenesis, but their impact on disease progression is still unclear. Our previous data show that astrocytes take up large amounts of aggregated amyloid-beta (A\u03b2) but are unable to successfully degrade the material, which is instead stored intracellularly. The aim of the present study was to analyze the astrocytic A\u03b2 deposits composition in detail in order to understand their role in AD propagation. For this purpose, human induced pluripotent cell (hiPSC)-derived astrocytes were exposed to sonicated A\u03b242 fibrils and magnetic beads. Live cell imaging and immunocytochemistry confirmed that the ingested A\u03b2 aggregates and beads were transported to the same lysosomal compartments in the perinuclear region, which allowed us to successfully isolate the A\u03b2 deposits from the astrocytes. Using a battery of experimental techniques, including mass spectrometry, western blot, ELISA and electron microscopy we demonstrate that human astrocytes truncate and pack the A\u03b2 aggregates in a way that makes them highly resistant. Moreover, the astrocytes release specifically truncated forms of A\u03b2 via different routes and thereby expose neighboring cells to pathogenic proteins. Taken together, our study establishes a role for astrocytes in mediating A\u03b2 pathology, which could be of relevance for identifying novel treatment targets for AD.", "doi": "10.1016/j.mcn.2024.103916", "pmid": "38244652", "labels": [], "xrefs": [{"db": "pii", "key": "S1044-7431(24)00001-0"}], "notes": [], "created": "2026-08-20T08:00:40.896Z", "modified": "2026-08-20T08:00:40.958Z"}], "created": "2026-08-20T08:00:40.922Z", "modified": "2026-08-20T08:00:40.922Z"}