https://www.frontiersin.org/articles/10.3389/fimmu.2016.00556/full

Emerging Roles for the Immune System in Traumatic Brain Injury

PDF File: https://www.frontiersin.org/articles/10.3389/fimmu.2016.00556/pdf?isPublishedV2=False

Traumatic brain injury (TBI) affects an ever-growing population of all ages with long-term consequences on health and cognition. Many of the issues that TBI patients face are thought to be mediated by the immune system. Primary brain damage that occurs at the time of injury can be exacerbated and prolonged for months or even years by chronic inflammatory processes, which can ultimately lead to secondary cell death, neurodegeneration, and long-lasting neurological impairment. Researchers have turned to rodent models of TBI in order to understand how inflammatory cells and immunological signaling regulate the post-injury response and recovery mechanisms. In addition, the development of numerous methods to manipulate genes involved in inflammation has recently expanded the possibilities of investigating the immune response in TBI models. As results from these studies accumulate, scientists have started to link cells and signaling pathways to pro- and anti-inflammatory processes that may contribute beneficial or detrimental effects to the injured brain. Moreover, emerging data suggest that targeting aspects of the immune response may offer promising strategies to treat TBI. This review will cover insights gained from studies that approach TBI research from an immunological perspective and will summarize our current understanding of the involvement of specific immune cell types and cytokines in TBI pathogenesis.

*Your macrophages and astroglia cells (astrocytes) can repair the brain after a TBI Traumatic Brain Injury

>>19525305

This article deals with Macrophages and Astrocytes, which repair the brain. Astrocytes, a.k.a astroglia cells…

https://www.frontiersin.org/articles/10.3389/fncel.2019.00528/full

Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets

PDF File: https://www.frontiersin.org/articles/10.3389/fncel.2019.00528/pdf?isPublishedV2=False

Traumatic brain injury (TBI) remains one of the leading causes of morbidity and mortality amongst civilians and military personnel globally. Despite advances in our knowledge of the complex pathophysiology of TBI, the underlying mechanisms are yet to be fully elucidated. While initial brain insult involves acute and irreversible primary damage to the parenchyma, the ensuing secondary brain injuries often progress slowly over months to years, hence providing a window for therapeutic interventions. To date, hallmark events during delayed secondary CNS damage include Wallerian degeneration of axons, mitochondrial dysfunction, excitotoxicity, oxidative stress and apoptotic cell death of neurons and glia. Extensive research has been directed to the identification of druggable targets associated with these processes. Furthermore, tremendous effort has been put forth to improve the bioavailability of therapeutics to CNS by devising strategies for efficient, specific and controlled delivery of bioactive agents to cellular targets. Here, we give an overview of the pathophysiology of TBI and the underlying molecular mechanisms, followed by an update on novel therapeutic targets and agents. Recent development of various approaches of drug delivery to the CNS is also discussed.

Astroglia/Astrocytes help to rebuild the myelin within the brain, treating MS and Parkinsons, to include a bunch of other issues of the brain and CNS (Central Nervous System)

*Astrocyte (from Ancient Greek ἄστρον, ástron, "star" + κύτος, kútos, "cavity", "cell")

>>19525316

This is a good one for our veterans and anyone who has been diagnosed with a TBI, Traumatic Brain Injury. Macrophages can help

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4210355/

Traumatic brain injury induces macrophage subsets in the brain

PDF File: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4210355/pdf/nihms633031.pdf

Traumatic brain injury (TBI) elicits innate inflammatory responses that can lead to secondary brain injury. To better understand the mechanisms involved in TBI-induced inflammation, we examined the nature of macrophages responding to TBI in mice. In this model, brain macrophages were increased >20-fold the day after injury and >77-fold four days after injury in the ipsilateral hemisphere compared with sham controls. TBI macrophage subsets were identified by using a reporter mouse strain (YARG) that expresses eYFP from an IRES inserted at the 3′ end of the gene for arginase-1 (Arg1), a hallmark of alternatively activated (M2) macrophages. One day after TBI, 21±1.5% of ipsilateral brain macrophages expressed relatively high levels of Arg1 as detected by YFP, and this subpopulation declined thereafter. Arg1+ cells localized with macrophages near the TBI lesion. Gene expression analysis of sorted Arg1+ and Arg1- brain macrophages revealed that both populations had profiles that included features of conventional M2 macrophages and classically activated (M1) macrophages. The Arg1+ cells differed from Arg1- cells in multiple aspects, most notably in their chemokine repertoires. Thus, the macrophage response to TBI initially involves heterogeneous polarization towards at least two major subsets.

my note*: You also have other types of macrophages in your brain, macroglia and microglia, your 'glial' cells, which his greek for "glue." You also possess astrocytes, which aid in repair of the brain and CNS (central nervous system), which is why GcMAF treats MS and Parkinsons to name a couple off the top of my head.

>>19525331

Some more helpful information, hopefully helpful to those who are dealing with a TBI, Traumatic Brain Injury.

https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-020-01778-5

The NLRP3 inflammasome in traumatic brain injury: potential as a biomarker and therapeutic target

PDF File: https://jneuroinflammation.biomedcentral.com/counter/pdf/10.1186/s12974-020-01778-5.pdf

Abstract

There is a great clinical need to identify the underlying mechanisms, as well as related biomarkers, and treatment targets, for traumatic brain injury (TBI). Neuroinflammation is a central pathophysiological feature of TBI. NLRP3 inflammasome activity is a necessary component of the innate immune response to tissue damage, and dysregulated inflammasome activity has been implicated in a number of neurological conditions. This paper introduces the NLRP3 inflammasome and its implication in the pathogenesis of neuroinflammatory-related conditions, with a particular focus on TBI. Although its role in TBI has only recently been identified, findings suggest that priming and activation of the NLRP3 inflammasome are upregulated following TBI. Moreover, recent studies utilizing specific NLRP3 inhibitors have provided further evidence that this inflammasome is a major driver of neuroinflammation and neurobehavioral disturbances following TBI. In addition, there is emerging evidence that circulating inflammasome-associated proteins may have utility as diagnostic biomarkers of neuroinflammatory conditions, including TBI. Finally, novel and promising areas of research will be highlighted, including the potential involvement of the NLRP3 inflammasome in mild TBI, how factors such as biological sex may affect NLRP3 activity in TBI, and the use of emerging biomarker platforms. Taken together, this review highlights the exciting potential of the NLRP3 inflammasome as a target for treatments and biomarkers that may ultimately be used to improve TBI management.

>>19525394

Chris Crispy

>>19525834

https://gab.com/Predestination/posts/110743068570733041

3 Threads of my compiled research, that includes videos, PDF files, graphs, pictures

All free for the taking… Your Immune system was the cure all along folks.

nagalase v. GcProtein.

nagalase destroys/breaks down GcProtein so that the body can't CONVERT it into GcMAF to fire up the immune system

>>19525997

I'm too old to care, that's my profile.