Reduced cerebral blood flow is associated with ageing, neurodegenerative disorders, and an increase in reactive oxygen species (ROS) formation.
There has been research into vitamin E's antioxidant and neuroprotective properties in Alzheimer's disease and other neurodegenerative disorders — it acts as a signalling and gene regulation molecule, and its half-life in the brain is long compared to other organs. Additionally, vitamin E deficiency is linked to cell damage, ataxia, impaired motor coordination, and cognitive dysfunction.
However, vitamin E's tocotrienols are poorly studied compared to its tocopherols. The former's anti-inflammatory activity has been reviewed, and they are said to be more effective when it comes to scavenging free radicals involved in neuro-inflammation.
The effects of E
Based on this, researchers at the International Islamic University Malaysia (IIUM)) and Egypt's Menoufia University conducted a study to evaluate vitamin E tocotrienol's anti-inflammatory and neuroprotective potential in rats with two-vessel occlusion (neuronal cell death in the hippocampus and cerebral cortex, the same structures affected during progressive neurodegeneration in Alzheimer's patients).
They divided 24 rats weighing between 200g and 250g equally into three groups: control, two-vessel occlusion (2VO, untreated) and 2VO+E (treated daily with 100mg/kg of oral ExcelVite's palm tocotrienol complex, EvNol).
After eight weeks, they were euthanised and their hippocampi isolated and examined.
The researchers observed that in the 2VO group, there was significantly higher neuronal cell death compared to the control group, and no significant difference in this regard between the treatment group and control group.
Additionally, the levels of isoprostanes — prominent oxidative stress biomarkers generated by lipid peroxidation and which further aggravate neuronal cell death — were also measured in all the rats.
The 2VO group was found to have markedly higher levels of isoprostanes compared to the control group, while the treatment group had significantly reduced isoprostane levels compared to the 2VO group.
The researchers therefore wrote: "This study demonstrates the effectiveness of vitamin E tocotrienol as a neuroprotective and antioxidant agent in chronic cerebral hypoperfusion-induced neurodegeneration in rats."
However, they added that the study had "important methodological limitations" due to the absence of an established antioxidant as a positive control, and its relatively small size.
They concluded: "The data provided in the study are preliminary in nature and need more exploration.
“For instance, it will be fruitful in future studies if we can measure gene expression and the protein expression of superoxide dismutase (SOD), LDH, as well as other stress markers in the different parts of the brain, including the cortex, hippocampus, and amygdala.
"Additionally, there is an urgent need to design studies on the lesser-known forms of vitamin E with the emphasis on the mode of action of vitamin E molecule in vivo. The outcome of such studies would yield rewarding returns."
Source: International Journal of Nutrition, Pharmacology, Neurological Diseases
"Oxidative Stress Status and Neuroprotection of Tocotrienols in Chronic Cerebral Hypoperfusion-Induced Neurodegeneration Rat Animal Model"
Authors: Wael M.Y. Mohamed, et al.