6th Edition of Neurology World Conference 2026

Abstract

War Veterans are particularly more prone to mental illnesses due to their prior encounters with multiple traumatic brain injuries (TBI) while serving on active duty, specifically in war zone areas. TBI is known to cause mortality or serious neurological disabilities among survivors. TBI has been previously reported to elicit several pathological processes, including neuroinflammation and blood-brain barrier (BBB) disruption, leading to secondary brain damage and the subsequent impairment of the neurovascular unit. Although several drugs have been shown to exhibit promising effects for TBI, the repertoire of currently available therapeutic strategies remains limited. Thymosin 4 (Tβ4) is a 43-amino acid G-acting sequestering peptide that has been previously documented to confer neuroprotective potential in TBI models. However, its role in BBB function remains unclear.

Further research into the mechanism of BBB disruption induced by TBI and its’ specific role in neurovascular pathophysiology is necessary. In the present study, the protective effects of Tβ4 in lipopolysaccharide (LPS)-stimulated gene expression of several tight junction proteins, inflammatory genes, apoptotic genes, and adhesion genes in human brain microvascular endothelial cells (hBMVECs), one of the pivotal cell types in the BBB, were reported. These data suggest that pre-treatment with Tβ4 reversed the LPS-induced damage of BBB components in hBMVECs. Furthermore, these results identified neuregulin 1 to be a possible target for Tβ4. Therefore, it can be proposed that Tβ4-mediated cellular signaling in hBMVEC may be vital for understanding the association between the BBB and TBI pathophysiology, which warrants further investigation.