Chronic traumatic encephalopathy: an update review

Chronic traumatic encephalopathy is a progressive neurodegenerative disease occurring in retired sportspersons who have received several head blows with concussions during their games. The clinical symptoms start with mood disorders and with a progressive evolution into dementia and Parkinsonism. The disease is due to a progressive accumulation of hyperphosphorilated tau in neurons as neurofibrillary tangles, abnormal neurites and inclusions in astrocytes around small vessels. There is a tendency of the lesions to occur in clusters at the sulcal depths of the cerebral cortex. Chronic traumatic encephalopathy has to be differentiated from Alzheimer’s disease, in which head trauma can also increase the illness symptoms. Recently, new tracers in positron emission topography of the brain have been used for a better evaluation of chronic traumatic encephalopathy. There is actually no treatment that allows to cure or to slowdown the evolution of chronic traumatic encephalopathy. However, new treatment studies are recently conducted and in progress.

EGCG Promotes Neurite Outgrowth through the Integrin β1/FAK/p38 Signaling Pathway after Subarachnoid Hemorrhage

The abnormal neurites have long been regarded as the main player contributing to the poor outcome of patients with subarachnoid hemorrhage (SAH). (-)-Eigallocatechin-3-gallate (EGCG), the major biological component of tea catechin, exhibited strong neuroprotective effects against central nervous system diseases; however, the role of EGCG-mediated neurite outgrowth after SAH has not been delineated. Here, the effect of reactive oxygen species (ROS)/integrin β1/FAK/p38 pathway on neurite outgrowth was investigated. As expected, oxyhemoglobin- (OxyHb-) induced excessive ROS level was significantly reduced by EGCG as well as antioxidant N-acetyl-l-cysteine (NAC). Consequently, the expression of integrin β1 was significantly inhibited by EGCG and NAC. Meanwhile, EGCG significantly inhibited the overexpression of phosphorylated FAK and p38 to basal level after SAH. As a result, the abnormal neurites and cell injury were rescued by EGCG, which eventually increased energy generation and neurological score after SAH. These results suggested that EGCG promoted neurite outgrowth after SAH by inhibition of ROS/integrin β1/FAK/p38 signaling pathway. Therefore, EGCG might be a new pharmacological agent that targets neurite outgrowth in SAH therapy.