Abstract
Alzheimer’s disease (AD) is plaguing the aging population worldwide due to its tremendous health care and socioeconomic burden. Current treatment of AD only offers symptomatic relief to patients. Development of agents targeting specific pathologies of AD is very slow. Tocotrienol, a member of the vitamin E family, can tackle many aspects of AD, such as oxidative stress, mitochondrial dysfunction and abnormal cholesterol synthesis. This review summarizes the current evidence on the role of tocotrienol as a neuroprotective agent. Preclinical studies showed that tocotrienol could reduce oxidative stress by acting as a free-radical scavenger and promoter of mitochondrial function and cellular repair. It also prevented glutamate-induced neurotoxicity in the cells. Human epidemiological studies showed a significant inverse relationship between tocotrienol levels and the occurrence of AD. However, there is no clinical trial to support the claim that tocotrienol can delay or prevent the onset of AD. As a conclusion, tocotrienol has the potential to be developed as an AD-preventing agent but further studies are required to validate its efficacy in humans.
Highlights
Alzheimer’s disease (AD) is a spectrum of neurodegenerative illnesses defined by clinical symptoms and biological changes in the brain
Since the neurobiological changes cannot be detected until post-mortem, diagnosis based on clinical symptoms alone is probabilistic and refers to as probable AD [1]
This review aims to summarize the current evidence of the effects of tocotrienols in AD
Summary
Alzheimer’s disease (AD) is a spectrum of neurodegenerative illnesses defined by clinical symptoms and biological changes in the brain. The characteristic clinical symptoms of AD include progressive dementia with episodic memory impairment. The biological changes refer to the presence of neurofibrillary entanglement, senile plaques, amyloid deposition and synaptic loss in the brain. Since the neurobiological changes cannot be detected until post-mortem, diagnosis based on clinical symptoms alone is probabilistic and refers to as probable AD [1]. With the progress in medical technology, in vivo detection of pathological changes in the brain directly via advanced imaging techniques (magnetic resonance imaging (MRI) and positron emission tomography (PET)). The combination of neuropsychological scores, neuroimaging and CSF biomarkers offers enhanced prediction on the development of AD in patients with mild cognitive impairment [4]
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