Serum ‘central nervous system specific’ protein biomarkers of traumatic brain injury

2015 ◽  
pp. 246-259
Author(s):  
Teresa M Evans ◽  
William E Haskins
Keyword(s):  
Traumatic Brain Injury ◽  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Specific Protein ◽  
Protein Biomarkers

scholarly journals Aggregated n-of-1 trials of central nervous system stimulants versus placebo for paediatric traumatic brain injury – a pilot study

Trials ◽  
2014 ◽  
Vol 15 (1) ◽  
Author(s):  
Catherine J Nikles ◽  
Lynne McKinlay ◽  
Geoffrey K Mitchell ◽  
Sue-Ann S Carmont ◽  
Hugh E Senior ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Pilot Study ◽  
Central Nervous System Stimulants

Central Nervous System Genomics

2011 ◽  
Vol 29 (1) ◽  
pp. 205-226 ◽  
Author(s):  
Matthew J. Gallek ◽  
Leslie Ritter
Keyword(s):  
Traumatic Brain Injury ◽  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Genomic Research ◽  
Nervous System Diseases ◽  
Central Nervous System Diseases ◽  
The Central Nervous System ◽  
Remarkable Progress ◽  
Made In

In the past 25 years, remarkable progress has been made in our understanding of genomics and its influence on central nervous system diseases. In this chapter, common diseases of the central nervous system will be reviewed along with the genomics associated with these diseases. The diseases/injuries that will be investigated include neurovascular disorders such as ischemic stroke, hemorrhagic stroke, subarachnoid hemorrhage, and traumatic brain injury. This chapter will also explore Apolipoprotein E (APOE), a 299-aminoacid protein encoded by the APOE gene, and its associations with many of the previously named diseases. APOE was first tied to the risk of Alzheimer's disease and has since then been investigated in traumatic brain injury and hemorrhagic strokes. In addition, we will discuss the future of genomic research in central nervous system diseases.

scholarly journals Therapeutic Neutralization of the NLRP1 Inflammasome Reduces the Innate Immune Response and Improves Histopathology after Traumatic Brain Injury

2009 ◽  
Vol 29 (7) ◽  
pp. 1251-1261 ◽  
Author(s):  
Juan Pablo de Rivero Vaccari ◽  
George Lotocki ◽  
Ofelia F Alonso ◽  
Helen M Bramlett ◽  
W Dalton Dietrich ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Inhibitor Of Apoptosis ◽  
Inhibitor Of Apoptosis Protein ◽  
Nlrp1 Inflammasome ◽  
Caspase 1 ◽  
Fluid Percussion Injury ◽  
Apoptosis Protein

Traumatic brain injury elicits acute inflammation that in turn exacerbates primary brain damage. A crucial part of innate immunity in the immune privileged central nervous system involves production of proinflammatory cytokines mediated by inflammasome signaling. Here, we show that the nucleotide-binding, leucine-rich repeat pyrin domain containing protein 1 (NLRP1) inflammasome consisting of NLRP1, caspase-1, caspase-11, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), the X-linked inhibitor of apoptosis protein, and pannexin 1 is expressed in neurons of the cerebral cortex. Moderate parasagittal fluid-percussion injury (FPI) induced processing of interleukin-1β, activation of caspase-1, cleavage of X-linked inhibitor of apoptosis protein, and promoted assembly of the NLRP1 inflammasome complex. Anti-ASC neutralizing antibodies administered immediately after fluid-percussion injury to injured rats reduced caspase-1 activation, X-linked inhibitor of apoptosis protein cleavage, and processing of interleukin-1β, resulting in a significant decrease in contusion volume. These studies show that the NLRP1 inflammasome constitutes an important component of the innate central nervous system inflammatory response after traumatic brain injury and may be a novel therapeutic target for reducing the damaging effects of posttraumatic brain inflammation.

Inhibition of the complement anaphylatoxin activities in the central nervous system disorders

2021 ◽  
Vol 21 (2) ◽  
pp. 37-52
Author(s):  
Kseniya A. Nekrasova ◽  
Alexander M. Ischenko ◽  
Alexander V. Trofimov
Keyword(s):  
Traumatic Brain Injury ◽  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Specific Activity ◽  
Craniocerebral Trauma ◽  
Epidemiological Data ◽  
Cerebrovascular Diseases ◽  
The Central Nervous System

The review is devoted to inhibition of the complement anaphylatoxin activities in diseases of the central nervous system. Here we present epidemiological data on the prevalence of cerebrovascular diseases, in particular, ischemic stroke and craniocerebral trauma. The mechanisms of complement activation and complement-mediated pathology in the central nervous system are considered in detail. Clinical data confirming the role of the complement system in the pathogenesis of stroke and of traumatic brain injury secondary injury are presented. We also summarize the results of in vivo specific activity studies of the complement anaphylatoxin inhibitors using animal models of stroke and traumatic brain injury. Briefly described is the present state of the art in developing drugs that target the effector compounds of the complement cascade.

Auditory Processing After Traumatic Brain Injury

2017 ◽  
Vol 2 (2) ◽  
pp. 147-151 ◽  
Author(s):  
Frederick J. Gallun
Keyword(s):  
Traumatic Brain Injury ◽  
Central Nervous System ◽  
Signal Processing ◽  
Nervous System ◽  
Brain Injury ◽  
Auditory System ◽  
Auditory Processing ◽  
The Other ◽  
Philosophical Question ◽  
Controlled Processing

Auditory processing involves many diverse aspects of the peripheral and central nervous system. Where “simple” transformation of information ends and “signal processing” begins is difficult to say with any certainty, and the distinction between “automatic” processing and “controlled” processing is an even more philosophical question. For these reasons, the damage that occurs in one portion of the nervous system can have serious implications for many other parts of the system. For this reason, it is essential that clinicians involved in working with patients for whom any portion of the auditory system is at risk need to be in close communication with those who specialize in understanding the other parts of this delicate and interwoven system.

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