Abstract
Alzheimer’s disease (AD) is an intractable neurodegenerative disease that leads to dementia, primarily in elderly people. The neurotoxicity of amyloid-beta (Aβ) and tau protein has been demonstrated over the last two decades. In line with these findings, several etiological hypotheses of AD have been proposed, including the amyloid cascade hypothesis, the oxidative stress hypothesis, the inflammatory hypothesis, the cholinergic hypothesis, et al. In the meantime, great efforts had been made in developing effective drugs for AD. However, the clinical efficacy of the drugs that were approved by the US Food and Drug Association (FDA) to date were determined only mild/moderate. We recently adopted a vanadium compound bis(ethylmaltolato)-oxidovanadium (IV) (BEOV), which was originally used for curing diabetes mellitus (DM), to treat AD in a mouse model. It was shown that BEOV effectively reduced the Aβ level, ameliorated the inflammation in brains of the AD mice, and improved the spatial learning and memory activities of the AD mice. These finding encouraged us to further examine the mechanisms underlying the therapeutic effects of BEOV in AD. In this review, we summarized the achievement of vanadium compounds in medical studies and investigated the prospect of BEOV in AD and DM treatment.
Highlights
Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders that is estimated to currently affect 50 million people, and this number is expected to triple by 2050 [1]
The mechanisms underlying the disfunction of glucose metabolism in both diseases may provide a new therapeutic approach for AD
The clinical studies showed that the vanadium compound truly improved the glucose uptake in diabetes mellitus (DM) patients; on the other hand, the experimental evidence showed that vanadium compounds could regulate the level of Ab in vivo and in vitro [12,15]
Summary
Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders that is estimated to currently affect 50 million people, and this number is expected to triple by 2050 [1]. Despite the intensive efforts in developing pharmaceutical agents for AD, only five have been approved by the US Food and Drug Administration (FDA) to date: cholinesterase inhibitors including Donepezil, Galantamine, and Rivastigmine, which could increase synaptic acetylcholine to improve learning and memory, and the NMDA receptor antagonist Memantine, as well as the most recently sanctified amyloid-beta (Aβ) oligomer monoclonal antibody, Aducanumab. The therapeutic effects of these agents are mild and quite controversial [2]. We examined the therapeutic effects of vanadium compound Bis(2-ethyl-3-hydroxy-4-pyronato) oxovanadium (IV) (BEOV), which was originally synthesized as a substitution of vanadate for curing diabetes mellitus (DM) in AD models. We found that BEOV significantly reduced the levels of Aβ and tau phosphorylation, and inhibited the inflammation induced by Aβ [13], blocked the endoplasmic reticulum (ER) stress induced neurotoxicity [14], and ameliorated the spatial learning and memory in AD mouse models [15]. We summarize the progress of the pharmacological research on vanadium compounds, and the emerging role of vanadium compounds in treating AD
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