Abstract
Vitamin E was proposed as treatment for Alzheimer’s disease many years ago. However, the effectiveness of the drug is not clear. Vitamin E is an antioxidant and neuroprotector and it has anti-inflammatory and hypocholesterolemic properties, driving to its importance for brain health. Moreover, the levels of vitamin E in Alzheimer’s disease patients are lower than in non-demented controls. Thus, vitamin E could be a good candidate to have beneficial effects against Alzheimer’s. However, evidence is consistent with a limited effectiveness of vitamin E in slowing progression of dementia; the information is mixed and inconclusive. The question is why does vitamin E fail to treat Alzheimer’s disease? In this paper we review the studies with and without positive results in Alzheimer’s disease and we discuss the reasons why vitamin E as treatment sometimes has positive results on cognition but at others, it does not.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a long evolution whose clinical symptoms appear late in life
In favor of this theory, we can say that the severity of this type of dementia correlates well with the growing accumulation of neurofibrillary tangles in the brain [11,12,13]; there is a high correlation between hyper-phosphorylated tau species in the cerebrospinal fluid (CSF) in patients with AD and the degree of cognitive impairment [14]; a decrease in tau filaments by drugs directed against this therapeutic target alleviates cognitive deterioration [15]
Lower levels of α-tocopherol but γ-tocopherol higher in serum of AD patients. They are less numerous, we can find other studies reported no difference in vitamin E levels (Table 2)
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a long evolution whose clinical symptoms appear late in life. We can divide the hypotheses into three groups: The hypotheses based on protein deposits This group includes the beta-amyloid (Aβ) cascade hypothesis; and the tau hypothesis. Neurons with a high content of hyper-phosphorylated tau enter into apoptosis and neurodegeneration takes place [10]. In favor of this theory, we can say that the severity of this type of dementia correlates well with the growing accumulation of neurofibrillary tangles in the brain [11,12,13]; there is a high correlation between hyper-phosphorylated tau species in the cerebrospinal fluid (CSF) in patients with AD and the degree of cognitive impairment [14]; a decrease in tau filaments by drugs directed against this therapeutic target alleviates cognitive deterioration [15]. It has been seen that the elevation of both cells and proinflammatory cytokines appears before the deposit of Aβ [20]
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