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Cis P-tau is induced in clinical and preclinical brain injury and contributes to post-injury sequelae

Author

Listed:
  • Onder Albayram

    (Harvard Medical School
    Harvard Medical School
    Harvard Medical School)

  • Asami Kondo

    (Harvard Medical School
    Harvard Medical School
    Harvard Medical School)

  • Rebekah Mannix

    (Harvard Medical School)

  • Colin Smith

    (University of Edinburgh)

  • Cheng-Yu Tsai

    (Harvard Medical School
    Harvard Medical School
    Harvard Medical School)

  • Chenyu Li

    (Harvard Medical School
    Harvard Medical School
    Harvard Medical School)

  • Megan K. Herbert

    (Harvard Medical School
    Harvard Medical School
    Harvard Medical School)

  • Jianhua Qiu

    (Harvard Medical School)

  • Michael Monuteaux

    (Harvard Medical School)

  • Jane Driver

    (Harvard Medical School
    Harvard Medical School)

  • Sandra Yan

    (Harvard Medical School)

  • William Gormley

    (Harvard Medical School)

  • Ava M. Puccio

    (University of Pittsburgh Medical Center)

  • David O. Okonkwo

    (University of Pittsburgh Medical Center)

  • Brandon Lucke-Wold

    (West Virginia University)

  • Julian Bailes

    (University of Chicago, Pritzker School of Medicine)

  • William Meehan

    (Harvard Medical School)

  • Mark Zeidel

    (Harvard Medical School)

  • Kun Ping Lu

    (Harvard Medical School
    Harvard Medical School
    Harvard Medical School)

  • Xiao Zhen Zhou

    (Harvard Medical School
    Harvard Medical School
    Harvard Medical School)

Abstract

Traumatic brain injury (TBI) is characterized by acute neurological dysfunction and associated with the development of chronic traumatic encephalopathy (CTE) and Alzheimer’s disease. We previously showed that cis phosphorylated tau (cis P-tau), but not the trans form, contributes to tau pathology and functional impairment in an animal model of severe TBI. Here we found that in human samples obtained post TBI due to a variety of causes, cis P-tau is induced in cortical axons and cerebrospinal fluid and positively correlates with axonal injury and clinical outcome. Using mouse models of severe or repetitive TBI, we showed that cis P-tau elimination with a specific neutralizing antibody administered immediately or at delayed time points after injury, attenuates the development of neuropathology and brain dysfunction during acute and chronic phases including CTE-like pathology and dysfunction after repetitive TBI. Thus, cis P-tau contributes to short-term and long-term sequelae after TBI, but is effectively neutralized by cis antibody treatment.

Suggested Citation

  • Onder Albayram & Asami Kondo & Rebekah Mannix & Colin Smith & Cheng-Yu Tsai & Chenyu Li & Megan K. Herbert & Jianhua Qiu & Michael Monuteaux & Jane Driver & Sandra Yan & William Gormley & Ava M. Pucci, 2017. "Cis P-tau is induced in clinical and preclinical brain injury and contributes to post-injury sequelae," Nature Communications, Nature, vol. 8(1), pages 1-17, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01068-4
    DOI: 10.1038/s41467-017-01068-4
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    Cited by:

    1. Sukanta Jash & Sayani Banerjee & Shibin Cheng & Bin Wang & Chenxi Qiu & Asami Kondo & Jan Ernerudh & Xiao Zhen Zhou & Kun Ping Lu & Surendra Sharma, 2023. "Cis P-tau is a central circulating and placental etiologic driver and therapeutic target of preeclampsia," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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