Widespread microglial activation in patients deceased from traumatic brain injury

Velázquez, Antonio Calonge; Ortega, M.; Rojas, Santiago; González-Oliván, Francisco Javier; Rodríguez‐Baeza, Alfonso

doi:10.3109/02699052.2015.1018325

Cited by 21 publications

(13 citation statements)

References 30 publications

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“…Clinical evidence supports the idea that microglial and macrophage activation occurs rapidly following TBI. In autopsy of patients who have died following severe TBI, activated microglial morphologies were detected 2-10 days after injury (Velazquez et al 2015). In addition, increased cerebrospinal fluid levels of ferritin and soluble CD163, markers of macrophage and microglial activation, were elevated in pediatric patients within 3 days of severe TBI (Newell et al 2015).…”

Section: Classic Examples Of Neuroinflammation In the Context Of Centmentioning

confidence: 99%

Neuroinflammation: the devil is in the details

DiSabato

Quan

Godbout

2016

Journal of Neurochemistry

1,087

737

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There is significant interest in understanding inflammatory responses within the brain and spinal cord. Inflammatory responses that are centralized within the brain and spinal cord are generally referred to as “neuroinflammatory”. Aspects of neuroinflammation vary within the context of disease, injury, infection or stress. The context, course, and duration of these inflammatory responses are all critical aspects in the understanding of these processes and their corresponding physiological, biochemical and behavioral consequences. Microglia, innate immune cells of the central nervous system (CNS), play key roles in mediating these neuroinflammatory responses. Because the connotation of neuroinflammation is inherently negative and maladaptive, the majority of research focus is on the pathological aspects of neuroinflammation. There are, however, several degrees of neuroinflammatory responses, some of which are positive. In many circumstances including CNS injury, there is a balance of inflammatory and intrinsic repair processes that influences functional recovery. In addition, there are several other examples where communication between the brain and immune system involves neuroinflammatory processes that are beneficial and adaptive. The purpose of this review is to distinguish different variations of neuroinflammation in a context-specific manner and detail both positive and negative aspects of neuroinflammatory processes.

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Section: Classic Examples Of Neuroinflammation In the Context Of Centmentioning

confidence: 99%

Neuroinflammation: the devil is in the details

DiSabato

Quan

Godbout

2016

Journal of Neurochemistry

1,087

737

View full text Add to dashboard Cite

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“…In the same model, immune cells from the periphery were also recruited to the site of injury prior to neurodegeneration and MHCII expression was found at later time points in the striatum, as the inclusion pathology spread across the synapse from dopaminergic neurons in the SNpc to medium spiny neurons of the striatum [50]. Similarly, following a TBI in humans, activated microglia expand throughout the injured brain regions [114,155]. In mice following a single controlled cortical impact, activated microglia and macrophages continue to express elevated levels of MHCII and CD68, a year after the injury [90].…”

Section: Inflammationmentioning

confidence: 99%

Biological links between traumatic brain injury and Parkinson’s disease

Delic

Beck

Pang

et al. 2020

acta neuropathol commun

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Parkinson's Disease (PD) is a progressive neurodegenerative disorder with no cure. Clinical presentation is characterized by postural instability, resting tremors, and gait problems that result from progressive loss of A9 dopaminergic neurons in the substantia nigra pars compacta. Traumatic brain injury (TBI) has been implicated as a risk factor for several neurodegenerative diseases, but the strongest evidence is linked to development of PD. Mild TBI (mTBI), is the most common and is defined by minimal, if any, loss of consciousness and the absence of significant observable damage to the brain tissue. mTBI is responsible for a 56% higher risk of developing PD in U.S. Veterans and the risk increases with severity of injury. While the mounting evidence from human studies suggests a link between TBI and PD, fundamental questions as to whether TBI nucleates PD pathology or accelerates PD pathology in vulnerable populations remains unanswered. Several promising lines of research point to inflammation, metabolic dysregulation, and protein accumulation as potential mechanisms through which TBI can initiate or accelerate PD. Amyloid precursor protein (APP), alpha synuclein (α-syn), hyper-phosphorylated Tau, and TAR DNA-binding protein 43 (TDP-43), are some of the most frequently reported proteins upregulated following a TBI and are also closely linked to PD. Recently, upregulation of Leucine Rich Repeat Kinase 2 (LRRK2), has been found in the brain of mice following a TBI. Subset of Rab proteins were identified as biological substrates of LRRK2, a protein also extensively linked to late onset PD. Inhibition of LRRK2 was found to be neuroprotective in PD and TBI models. The goal of this review is to survey current literature concerning the mechanistic overlap between TBI and PD with a particular focus on inflammation, metabolic dysregulation, and aforementioned proteins. This review will also cover the application of rodent TBI models to further our understanding of the relationship between TBI and PD.

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“…Studies have also demonstrated neuroinflammation in various brain regions within the human population following TBI [119][120][121][122] . Molecular imaging studies have demonstrated microglial activation in populations of TBI patients as visualized via positron emission tomography using ligands for the mitochondrial translocator protein, TSPO, following brain injury [114,[119][120][121] .…”

Section: Neuroinflammation In Tbimentioning

confidence: 99%

Microglial process convergence on axonal segments in health and disease

Benusa

Lafrenaye

2020

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Microglia dynamically interact with neurons influencing the development, structure, and function of neuronal networks. Recent studies suggest microglia may also influence neuronal activity by physically interacting with axonal domains responsible for action potential initiation and propagation. However, the nature of these microglial process interactions is not well understood. Microglial-axonal contacts are present early in development and persist through adulthood, implicating microglial interactions in the regulation of axonal integrity in both the developing and mature central nervous system. Moreover, changes in microglial-axonal contact have been described in disease states such as multiple sclerosis (MS) and traumatic brain injury (TBI). Depending on the disease state, there are increased associations with specific axonal segments. In MS, there is enhanced contact with the axon initial segment and node of Ranvier, while, in TBI, microglia alter interactions with axons at the site of injury, as well as at the axon initial segment. In this article, we review the interactions of microglial processes with axonal segments, analyzing their associations with various axonal domains and how these interactions may differ between MS and TBI. Furthermore, we discuss potential functional consequences and molecular mechanisms of these interactions and how these may differ among various types of microglial-axonal interactions.

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Widespread microglial activation in patients deceased from traumatic brain injury

Abstract: The findings indicate that TBI induces a widespread activation of brain microglia which affects all cortical areas, including those distant from the contusion site.

Cited by 21 publications

References 30 publications

Neuroinflammation: the devil is in the details

Neuroinflammation: the devil is in the details

Biological links between traumatic brain injury and Parkinson’s disease

Microglial process convergence on axonal segments in health and disease

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