Our interests in vitamin E has been primarily in the form of tocotrienol – a lesser known form of vitamin E. The findings that minute amount of tocotrienol has been found to be extremely neuroprotective than the common form of vitamin E tocopherol. In a large animal study has shown that tocotrienol is not only neuroprotective, but tocotrienol also promotes blood flow to the stroke infected site. There are four major molecular checkpoints that account for brain cell death protection mechanisms. In addition, a new mechanism has been identified in relation to the improved blood flow to the affected site. Taken together, tocotrienol may have possess multi-prong approach to mitigate cerebra small vascular disease. These findings are very encouraging because tocotrienol as naturally design molecule that targets multiple targets towards a common outcome – cerebra small vessel disease protection.
Below are some of the relevant references:
Large animal study
- Rink, C. et.al (2011). Tocotrienol vitamin E protects against preclinical canine ischemic stroke by inducing arteriogenesis. J Cereb Blood Flow Metab.
Four Molecular Checkpoints
- Sen C.K., et.al (2000). Molecular basis of vitamin E action. Tocotrienol potently inhibits glutamate-induced pp60(c-Src) kinase activation and death of HT4 neuronal cells. J Biol Chem.
- Khanna, S., et.al (2003). Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegeneration. J Biol Chem.
- Khanna, S., et.al (2010). Nanomolar vitamin E alpha-tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection. J Neurochem.
- Khanna S., et.al (2013). Loss of miR-29b following acute ischemic stroke contributes to neural cell death and infarct size. J Cereb Blood Flow Metab.