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Amyloid beta acts synergistically as a pro-inflammatory cytokine. | LitMetric

Amyloid beta acts synergistically as a pro-inflammatory cytokine.

Neurobiol Dis

Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO, United States of America. Electronic address:

Published: November 2021

AI Article Synopsis

  • The amyloid beta (Aβ) peptide is linked to Alzheimer's disease and its natural functions are not fully understood.
  • This study finds that low concentrations of Aβ enhance inflammation in human astrocytes when combined with other cytokines, indicating it may play a role similar to cytokines in immune activation.
  • Additionally, astrocytes activated by Aβ show a gene expression pattern similar to harmful "A1" astrocytes that are associated with aging and Alzheimer's disease, suggesting Aβ contributes to neuroinflammation in a novel way.

Article Abstract

The amyloid beta (Aβ) peptide is believed to play a central role in Alzheimer's disease (AD), the most common age-related neurodegenerative disorder. However, the natural, evolutionarily selected functions of Aβ are incompletely understood. Here, we report that nanomolar concentrations of Aβ act synergistically with known cytokines to promote pro-inflammatory activation in primary human astrocytes (a cell type increasingly implicated in brain aging and AD). Using transcriptomics (RNA-seq), we show that Aβ can directly substitute for the complement component C1q in a cytokine cocktail previously shown to induce astrocyte immune activation. Furthermore, we show that astrocytes synergistically activated by Aβ have a transcriptional signature similar to neurotoxic "A1" astrocytes known to accumulate with age and in AD. Interestingly, we find that this biological action of Aβ at low concentrations is distinct from the transcriptome changes induced by the high/supraphysiological doses of Aβ often used in in vitro studies. Collectively, our results suggest an important, cytokine-like function for Aβ and a novel mechanism by which it may directly contribute to the neuroinflammation associated with brain aging and AD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8502211PMC
http://dx.doi.org/10.1016/j.nbd.2021.105493DOI Listing

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