Neuroprotective Strategies for Traumatic Brain Injury: Improving Clinical Translation

Abstract

Traumatic brain injury (TBI) induces secondary biochemical changes that contribute to delayed neuroinflammation, neuronal cell death, and neurological dysfunction. Attenuating such secondary injury has provided the conceptual basis for neuroprotective treatments. Despite strong experimental data, more than 30 clinical trials of neuroprotection in TBI patients have failed. In part, these failures likely reflect methodological differences between the clinical and animal studies, as well as inadequate pre-clinical evaluation and/or trial design problems. However, recent changes in experimental approach and advances in clinical trial methodology have raised the potential for successful clinical translation. Here we critically analyze the current limitations and translational opportunities for developing successful neuroprotective therapies for TBI.

The Photobiomodulatory Therapy and ILIB in the Repair of Encephalic Cisterns and Progressive Cognitive Restoration in a Patient with Traumatic Brain Injury

“…The results were measured by the Rancho los Amigos Cognitive Levels Scale [5][6][7][8][9][10][11][12][13][14][15][16][17], represented by the state of agitation or inappropriateness and functional capacity, divided into ten levels, which assign values to the different levels of brain function, according to the patient's reaction to external stimuli. In this study, the patient reached an evolution from level 1 to level 3, and reestablishment of brain cisterns (axial section) in the image examination …”

“…Secondary lesions may be due to inflammation, glutamate excitotoxicity, cell necrosis, glial proliferation, mitochondrial dysfunction, apoptosis, and oxygen free radical production and diffuse axonal injury [12][13][14][15]. These pathological alterations result in changes in synaptogenesis, dendritic remodeling and neurogenesis in the cortical and limbal regions of the hippocampus, prefrontally [16].…”

Brain and Exercise: Review

“…moleküller üzerinde de durulmaktadır. 40 Progesteron, glutamat toksisitesinde, lipit peroksidasyonunda azalma sağlayarak, statinler TNF-α, hücre adezyon molekülü-1 yanıtlarında baskılanma yaparak, siklosporin-A ise mitokondriyal fonksiyonları koruyarak ve oksidatif stresi baskılayarak etki yaptığı düşünülen ve nörodejenerasyonu azaltabileceğine inanılan moleküllerdir.…”

Traumatic Brain Injury: An Update

“…Specifically, this effort has focused on the mitigation of the role of various pathways involved in the pathogenesis of the secondary brain injury. Among others, the potential neuroprotective roles of calcium-channel antagonists 13 ; steroids 14 ; N-methyl-D-aspartate (NMDA) antagonists 15,16 ; glutamate agonists 17 ; oxygen free-radical scavengers 18 ; immune-modulators 19,20 ; statins …”