Traumatic brain injury (TBI) is one of the most important clinical issues, ranks as the sixth leading cause of death and results in economic loss of over ten billion NTD per year. The mechanisms for which TBI leads to degenerative diseases such as dementia are intriguing. Recent studies revealed that the activation of histone deacetylase (HDAC) and Glycogen systhase kinase 3 (GSK-3) after TBI might contribute to injurious effects (Dash et al., 2011). While several agents demonstrate therapeutic effects via pathways involving HDAC and GSK-3, evidences regarding therapeutic clinical effects after TBI involving these potential agents are lacking. Valproate (VPA) and lithium are two of the possible therapeutic agents for TBI. VPA is a HDAC inhibitor commonly used for treatment of epilepsy. It is reported that VPA can provide neuroprotection and improve cognitive function in TBI rat model. While VPA has demonstrated neuroprotective effects in animals, its role in providing clinical improvement awaits further study. Also, adverse effects of VPA treatment should be taken into consideration prior to staring the standard care for TBI patients. In this study, we aim to investigate the new clinical therapeutic effects of VPA in TBI patients.
|Effective start/end date||8/7/14 → 8/6/16|
- Traumatic brain injury