Deregulation of Sleep/Wake Homeostasis by Binge Alcohol Use Following Traumatic Brain Injury

创伤性脑损伤后酗酒导致睡眠/觉醒稳态失调

基本信息

  • 批准号:
    10527774
  • 负责人:
  • 金额:
    $ 20.66万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2022
  • 资助国家:
    美国
  • 起止时间:
    2022-08-15 至 2024-05-31
  • 项目状态:
    已结题

项目摘要

SUMMARY The sleep/wake cycle is regulated by the brain’s master circadian clock. Sleep disturbance is common in the general population and prominent in patients of neuropathological diseases. Notably, binge alcohol use (BAU) and traumatic brain injury (TBI) represent two of the strongest environmental risk factors for neurological disabilities. While cognitive deficits remain the cardinal manifestation of BAU/TBI pathology, non-cognitive homeostatic abnormalities are an integral part of the disease. A common symptom in TBI and BAU is sleep/wake disturbance, especially later in life, which often precedes cognitive decline to drive pathology and contributes to cognitive dysfunction. Thus, sleep/wake homeostasis can be both a culprit and target for therapeutic intervention, but represents a major missed opportunity not only in basic research but also for clinical practice. This is due to the limited understanding of the cause-effect between chronic TBI/ BAU pathology and circadian/sleep dysfunction. Recent studies (including our own) show that the proinflammatory NF-kB pathway, a key driver of inflammation, directly interacts with the core clock component BMAL1 and interferes with clock function across cell and tissue types and in locomotor activity rhythms. Further, NF-kB activation also alters sleep quantity and quality. These findings, together with the well-recognized sleep-neuroimmune interactions, support our central hypothesis that TBI/BAU comorbid neuroinflammation and neuropathology cause circadian and sleep disruption. The proposed research will determine for the first time the lifelong timeline (acute, subacute, chronic) of TBI/BAU neuropathology and sleep dysfunction, which will allow us to identify the key time windows of pathogenesis and sleep/wake phenotypes. For this, we will combine neuropathological analysis with non-invasive longitudinal sleep assays. This study will lay the groundwork for future molecular and genomic studies on how TBI and BAU induce neuroinflammation and how neuroinflammation impacts circadian and sleep homeostasis. This research will have broad implications in a number of neuropathological conditions that have an inflammatory component.
总结

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Andrew C. Liu其他文献

Sleep Disruption in a Mouse Model of Chronic Traumatic Brain Injury
慢性创伤性脑损伤小鼠模型的睡眠中断
  • DOI:
  • 发表时间:
    2023
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Andrew R. Morris;Erwin K. Gudenschwager Basso;Miguel A. Gutierrez;Rawad Daniel Arja;Firas Kobeissy;Christopher G. Janus;Kevin K. Wang;Jiepei Zhu;Andrew C. Liu
  • 通讯作者:
    Andrew C. Liu
Circadian rhythm defects in Prader-Willi syndrome neurons
普拉德-威利综合征神经元的昼夜节律缺陷
  • DOI:
    10.1016/j.xhgg.2025.100423
  • 发表时间:
    2025-04-10
  • 期刊:
  • 影响因子:
    3.600
  • 作者:
    A. Kaitlyn Victor;Tayler Hedgecock;Chidambaram Ramanathan;Yang Shen;Andrew C. Liu;Lawrence T. Reiter
  • 通讯作者:
    Lawrence T. Reiter

Andrew C. Liu的其他文献

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{{ truncateString('Andrew C. Liu', 18)}}的其他基金

Role of mTOR in Circadian and Sleep Deregulation in Smith-Kingsmore Syndrome (SKS)
mTOR 在史密斯-金斯莫尔综合征 (SKS) 昼夜节律和睡眠失调中的作用
  • 批准号:
    10586191
  • 财政年份:
    2023
  • 资助金额:
    $ 20.66万
  • 项目类别:
Deregulation of Sleep/Wake Homeostasis by Binge Alcohol Use Following Traumatic Brain Injury
创伤性脑损伤后酗酒导致睡眠/觉醒稳态失调
  • 批准号:
    10683216
  • 财政年份:
    2022
  • 资助金额:
    $ 20.66万
  • 项目类别:

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