David J. Loane, PhD, Trinity College Dublin, Ireland
Lee A Shapiro, PhD, Texas A&M University College of Medicine, United States of America
Journal of Neuroinflammation is calling for submissions to our Collection on "Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury".
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Traumatic brain injury (TBI) is a significant risk factor for Alzheimer’s disease (AD), and accumulating evidence supports a role for adaptive immune B and T cells in both TBI and AD pathogenesis. We previousl...
Repetitive mild traumatic brain injuries (rmTBI) sustained within a window of vulnerability can result in long term cognitive deficits, depression, and eventual neurodegeneration associated with tau pathology,...
Uncontrolled neuroinflammation mediates traumatic brain injury (TBI) pathology and impairs recovery. Interleukin-6 (IL-6), a pleiotropic inflammatory regulator, is associated with poor clinical TBI outcomes. I...
White matter injury (WMI) represents a significant etiological factor contributing to neurological impairment subsequent to Traumatic Brain Injury (TBI). CD36 receptors are recognized as pivotal participants i...
The gut microbiota plays a critical role in regulating brain function through the microbiome-gut-brain axis (MGBA). Dysbiosis of the gut microbiota is associated with neurological impairment in Traumatic brain...
The lectin pathway (LP) of complement mediates inflammatory processes linked to tissue damage and loss of function following traumatic brain injury (TBI). LP activation triggers a cascade of proteolytic events...
Perihematomal edema (PHE) after post-intracerebral hemorrhage (ICH) has complex pathophysiological mechanisms that are poorly understood. The complicated immune response in the post-ICH brain constitutes a cru...
Traumatic brain injury (TBI) is a major cause of disability and mortality worldwide, particularly among the elderly, yet our mechanistic understanding of what renders the post-traumatic brain vulnerable to poo...
Epidemiological studies have unveiled a robust link between exposure to repetitive mild traumatic brain injury (r-mTBI) and elevated susceptibility to develop neurodegenerative disorders, notably chronic traum...
Traumatic brain injury (TBI) is a chronic and debilitating disease, associated with a high risk of psychiatric and neurodegenerative diseases. Despite significant advancements in improving outcomes, the lack o...
Pneumonia is a common comorbidity in patients with severe traumatic brain injury (TBI), and is associated with increased morbidity and mortality. In this study, we established a model of intratracheal Klebsiella ...
Obesity increases the morbidity and mortality of traumatic brain injury (TBI). Detailed analyses of transcriptomic changes in the brain and adipose tissue were performed to elucidate the interactive effects be...
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 (...
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...
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...
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...
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...
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...
The Correction to this article has been published in Journal of Neuroinflammation 2023 20:287
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...
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...
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...
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...
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
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.