How does amyloid beta alter levels of ınflammation parameters in human astrocyte culture?

Background In neurodegenerative diseases, specific neuron types and glial cells undergo degeneration leading to the appearance of specific disease symptoms (1). Neurodegenerative diseases in the central nervous system (CNS) are also highly effective on cells that support neuron life. Astrocytes are...

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Published in:Alzheimer's & dementia 2023-12, Vol.19 (S13), p.n/a
Main Authors: Şengül, Büşra, Keskin, Ebru, Dursun, Erdinc, Gezen‐Ak, Duygu
Format: Article
Language:English
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Summary:Background In neurodegenerative diseases, specific neuron types and glial cells undergo degeneration leading to the appearance of specific disease symptoms (1). Neurodegenerative diseases in the central nervous system (CNS) are also highly effective on cells that support neuron life. Astrocytes are dynamic support cells that maintain brain balance, regulate the neurotransmitter system, process synaptic information, energy metabolism, antioxidant system, and inflammatory response (2). The blood‐brain barrier (BBB) may lose its permeability in pathological conditions. Both endothelial cells and astrocytes undergo phenotypic changes and become reactive (3). In Alzheimer’s disease (AD), amyloid beta (Aβ) is suggested to induce a pathological pathway that leads to neurodegeneration and dementia (4). A limited number of studies in the literature reveal a general profile of the neuroinflammatory mediators induced by Aβ, one of the main pathological elements of AD in human astrocytes. Method Based on this information, AD‐like pathology was created in our study with Aβ1‐42 treatment in human astrocyte cultures. The inflammatory response of these pathologies in human astrocytes was compared with the profile that emerges differently from a healthy astrocyte population. Alterations in the levels of released inflammatory proteins and their receptors were detected with the chemiluminescence‐based Western/dot blot method by using the human inflammation antibody array (Ray Biotech C‐Series Human Antibody Inflammation Array C4). Result Our data show that Aβ1‐42 treatment predominantly releases IL‐6, MCP‐1, and TIMP‐2 proteins into the culture supernatant in human astrocyte cells. On the other hand, whether reactive astrogliosis was triggered in the presence of Aβ in human astrocytes was followed by immunofluorescent labeling (IF). Conclusion This is the first study that investigated the general profile of released inflammatory factors in human astrocytes and how this profile is altered by Aβ1‐42 treatment. (The present work was supported by the Research Fund of Istanbul University, Project no: 30666)
ISSN:1552-5260
1552-5279
DOI:10.1002/alz.076600