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Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury

Guest Editors:
David J. Loane:
Trinity College Dublin, Ireland
Lee A Shapiro: Texas A&M University College of Medicine, USA

Submission Status: Open   |   Submission Deadline: 15 February 2024

Journal of Neuroinflammation is calling for submissions to our Collection on "Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury".

Image credit: idealeksis /

About the collection

The neuroinflammatory hypothesis of traumatic brain injury (TBI) broadly states that neuroinflammatory mechanisms underlie many of the negative sequela of TBI. Each year, millions of people experience a TBI, with worldwide estimates suggesting as many as 69 million people suffer a TBI annually. In the United States alone, more than 40 million Americans over 40 years of age are living with TBI. Suffering a TBI increases the 30-year mortality rate by 2.2 – 2.9x, and it frequently induces depression, cognitive impairment, and other neurobehavioral dysfunction. TBI also increases susceptibility to acute and chronic neurodegenerative disorders, including epilepsy, Parkinson’s disease, and Alzheimer’s disease. Although clinical trials for TBI biomarkers and therapeutics have largely failed, major advances in the identification of functional neuroimmune and neuroinflammatory mechanisms hold renewed promise as important post-traumatic therapeutic targets. This Collection seeks to explore these novel functional mechanisms after TBI with an eye towards elucidating and modifying the pathogenic progression to the various post-traumatic syndromes.

As part of this Collection, we invite articles that include:

• Innate immune and neuroimmune mechanisms, including DAMP’s and complement signaling
• Adaptive immune and neuroimmune mechanisms
• Meningeal lymphatics, glymphatic, lymphatic dysfunction in TBI
• Gut/neuroinflammatory axis
• Vascular/neuroimmune axis
• Immune cell/brain cell interactions
• Immunometabolism and TBI
• Neuroinflammatory biomarkers of TBI severity and outcomes
• Sex as a biological variable in the neuroimmune response to injury
• Translational human immune mechanisms
• Astrocyte and microglial mechanisms and function

  1. Traumatic encephalopathy syndrome (TES) is defined as the clinical manifestation of the neuropathological entity chronic traumatic encephalopathy (CTE). A core feature of TES is neurobehavioral dysregulation (...

    Authors: Suzan van Amerongen, Surya V. Pulukuri, Fatima Tuz-Zahra, Yorghos Tripodis, Jonathan D. Cherry, Charles Bernick, Yonas E. Geda, Jennifer V. Wethe, Douglas I. Katz, Michael L. Alosco, Charles H. Adler, Laura J. Balcer, Nicholas J. Ashton, Kaj Blennow, Henrik Zetterberg, Daniel H. Daneshvar…
    Citation: Journal of Neuroinflammation 2024 21:46
  2. Monocytes represent key cellular elements that contribute to the neurological sequela following brain injury. The current study reveals that trauma induces the augmented release of a transcriptionally distinct...

    Authors: Erwin K. Gudenschwager Basso, Jing Ju, Eman Soliman, Caroline de Jager, Xiaoran Wei, Kevin J. Pridham, Michelle L. Olsen and Michelle H. Theus
    Citation: Journal of Neuroinflammation 2024 21:41
  3. Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological respons...

    Authors: Tamara L. Baker, David K. Wright, Alessandro D. Uboldi, Christopher J. Tonkin, Anh Vo, Trevor Wilson, Stuart J. McDonald, Richelle Mychasiuk, Bridgette D. Semple, Mujun Sun and Sandy R. Shultz
    Citation: Journal of Neuroinflammation 2024 21:14
  4. Efferocytosis is a process that removes apoptotic cells and cellular debris. Clearance of these cells alleviates neuroinflammation, prevents the release of inflammatory molecules, and promotes the production o...

    Authors: Eman Soliman, John Leonard, Erwin Kristobal Gudenschwager Basso, Ilana Gershenson, Jing Ju, Jatia Mills, Caroline de Jager, Alexandra M. Kaloss, Mohamed Elhassanny, Daniela Pereira, Michael Chen, Xia Wang and Michelle H. Theus
    Citation: Journal of Neuroinflammation 2023 20:256
  5. Childhood represents a period of significant growth and maturation for the brain, and is also associated with a heightened risk for mild traumatic brain injuries (mTBI). There is also concern that repeated-mTB...

    Authors: Katie J. Neale, Hannah M. O. Reid, Barbara Sousa, Erin McDonagh, Jamie Morrison, Sandy Shultz, Eric Eyolfson and Brian R. Christie
    Citation: Journal of Neuroinflammation 2023 20:250
  6. Neuroinflammation contributes to secondary injury cascades following traumatic brain injury (TBI), with alternating waves of inflammation and resolution. Interleukin-1 (IL-1), a critical neuroinflammatory medi...

    Authors: Jonathan C. Vincent, Colleen N. Garnett, James B. Watson, Emma K. Higgins, Teresa Macheda, Lydia Sanders, Kelly N. Roberts, Ryan K. Shahidehpour, Eric M. Blalock, Ning Quan and Adam D. Bachstetter
    Citation: Journal of Neuroinflammation 2023 20:248

    The Correction to this article has been published in Journal of Neuroinflammation 2023 20:287

  7. Traumatic brain injury (TBI) is a significant worldwide public health concern that necessitates attention. Apoptosis signal-regulating kinase 1 (ASK1), a key player in various central nervous system (CNS) dise...

    Authors: Shan Meng, Hui Cao, Yichen Huang, Ziyu Shi, Jiaying Li, Yana Wang, Yue Zhang, Shuning Chen, Hong Shi and Yanqin Gao
    Citation: Journal of Neuroinflammation 2023 20:244
  8. Understanding the microglial neuro-immune interactions in the primate brain is vital to developing therapeutics for cortical injury, such as stroke or traumatic brain injury. Our previous work showed that mese...

    Authors: Yuxin Zhou, Hrishti Bhatt, Chromewell A. Mojica, Hongqi Xin, Monica A. Pessina, Douglas L. Rosene, Tara L. Moore and Maria Medalla
    Citation: Journal of Neuroinflammation 2023 20:201
  9. Individuals who have experienced mild traumatic brain injuries (mTBIs) suffer from several comorbidities, including chronic pain. Despite extensive studies investigating the underlying mechanisms of mTBI-assoc...

    Authors: Tyler Nguyen, Natalie Nguyen, Ashlyn G. Cochran, Jared A. Smith, Mohammed Al-Juboori, Andrew Brumett, Saahil Saxena, Sarah Talley, Edward M. Campbell, Alexander G. Obukhov and Fletcher A. White
    Citation: Journal of Neuroinflammation 2023 20:196
  10. Traumatic brain injury (TBI) remains a major cause of death and severe disability worldwide. We found previously that treatment with exogenous naïve B cells was associated with structural and functional neurop...

    Authors: Liam J. Dwyer, Saumya Maheshwari, Emily Levy, Mark C. Poznansky, Michael J. Whalen and Ruxandra F. Sîrbulescu
    Citation: Journal of Neuroinflammation 2023 20:133

Submission Guidelines

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This Collection welcomes submission of original Research Articles. Should you wish to submit a different article type, please read our submission guidelines to confirm that type is accepted by the journal. Articles for this Collection should be submitted via our submission system, Snapp. During the submission process you will be asked whether you are submitting to a Collection, please select "Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury" from the dropdown menu.

Articles will undergo the journal’s standard peer-review process and are subject to all of the journal’s standard policies. Articles will be added to the Collection as they are published.

The Guest Editors have no competing interests with the submissions which they handle through the peer review process. The peer review of any submissions for which the Guest Editors have competing interests is handled by another Editorial Board Member who has no competing interests.