Abstract
Neurodegenerative disorders, such as Parkinson's and Alzheimer's disease, are claimed to be of major concern causing a significant disease burden worldwide. Oxidative stress, mitochondrial dysfunction and nerve damage are the main reasons for the emergence of these diseases. The formation of reactive oxygen species (ROS) is the common chemical molecule that is formed from all these three interdependent mechanisms which is highly reactive toward the neuronal cells. For these reasons, the administration of tocotrienols (T3s), which is a potent antioxidant, is proven to cater to this problem, through in vitro and in vivo investigations. Interestingly, their therapeutic potentials are not only limited to antioxidant property but also to being able to reverse the neuronal damage and act as a shield for mitochondria dysfunction. Thereby, T3s prevents the damage to the neurons. In regards to this statement, in this review, we focused on summarizing and discussing the potential therapeutic role of T3s on Alzheimer's and Parkinson's diseases, and their protective mechanisms based on evidence from the in vitro and in vivo studies. However, there is no clinical trial conducted to prove the efficacy of T3s for Alzheimer's and Parkinson's subjects. As such, the therapeutic role of T3s for these neurodegenerative disorders is still under debate.
Highlights
Over the past 25 years, neurodegenerative disorders, such as Alzheimer’s (AD), Parkinson’s (PD), and Huntington (HD) diseases, are on the upsurge due to longer life expectancy, as age is one of the risk factors when contracting any one of these diseases [1]
Due to the complex pathogenesis of neurodegenerative disorders, detecting and treating the disorders remain as a challenging task despite the existence of a wide range of modern technologies and medicine [2]
T3s-rich fraction (TRF) decreases the activity of lipid peroxidase and inhibits its binding toward the DNA in neuronal cells of myoblasts, preventing oxidative damage to the DNA [56]
Summary
Over the past 25 years, neurodegenerative disorders, such as Alzheimer’s (AD), Parkinson’s (PD), and Huntington (HD) diseases, are on the upsurge due to longer life expectancy, as age is one of the risk factors when contracting any one of these diseases [1]. In PD, oxidative stress leads to misfolding of α-synuclein protein that causes neurodegeneration; loss of dopaminergic neurons and loss of dopamine in the brain [20]. This contributes to the damage of complex I activity, eventually to mitochondrial dysfunction and increased oxidative stress.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
