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Overexpression of endophilin A1 exacerbates synaptic alterations in a mouse model of Alzheimer’s disease

Author

Listed:
  • Qing Yu

    (University of Kansas
    Sichuan University)

  • Yongfu Wang

    (University of Kansas)

  • Fang Du

    (University of Kansas)

  • Shijun Yan

    (University of Kansas)

  • Gang Hu

    (University of Kansas)

  • Nicola Origlia

    (Institute of Neuroscience)

  • Grazia Rutigliano

    (Institute of Neuroscience)

  • Qinru Sun

    (University of Kansas)

  • Haiyang Yu

    (Sichuan University)

  • James Ainge

    (University of St Andrews)

  • Shi Fang Yan

    (University of Kansas)

  • Frank Gunn-Moore

    (University of St Andrews)

  • Shirley ShiDu Yan

    (University of Kansas)

Abstract

Endophilin A1 (EP) is a protein enriched in synaptic terminals that has been linked to Alzheimer’s disease (AD). Previous in vitro studies have shown that EP can bind to a variety of proteins, which elicit changes in synaptic transmission of neurotransmitters and spine formation. Additionally, we previously showed that EP protein levels are elevated in AD patients and AD transgenic animal models. Here, we establish the in vivo consequences of upregulation of EP expression in amyloid-β peptide (Aβ)-rich environments, leading to changes in both long-term potentiation and learning and memory of transgenic animals. Specifically, increasing EP augmented cerebral Aβ accumulation. EP-mediated signal transduction via reactive oxygen species (ROS)/p38 mitogen-activated protein (MAP) kinase contributes to Aβ-induced mitochondrial dysfunction, synaptic injury, and cognitive decline, which could be rescued by blocking either ROS or p38 MAP kinase activity.

Suggested Citation

  • Qing Yu & Yongfu Wang & Fang Du & Shijun Yan & Gang Hu & Nicola Origlia & Grazia Rutigliano & Qinru Sun & Haiyang Yu & James Ainge & Shi Fang Yan & Frank Gunn-Moore & Shirley ShiDu Yan, 2018. "Overexpression of endophilin A1 exacerbates synaptic alterations in a mouse model of Alzheimer’s disease," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04389-0
    DOI: 10.1038/s41467-018-04389-0
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