Abstract
The available drug therapy for post-ischemic neurodegeneration of the brain is symptomatic. This review provides an evaluation of possible dietary therapy for post-ischemic neurodegeneration with myricetin. The purpose of this review was to provide a comprehensive overview of what scientists have done regarding the benefits of myricetin in post-ischemic neurodegeneration. The data in this article contribute to a better understanding of the potential benefits of myricetin in the treatment of post-ischemic brain neurodegeneration, and inform physicians, scientists and patients, as well as their caregivers, about treatment options. Due to the pleiotropic properties of myricetin, including anti-amyloid, anti-phosphorylation of tau protein, anti-inflammatory, anti-oxidant and autophagous, as well as increasing acetylcholine, myricetin is a promising candidate for treatment after ischemia brain neurodegeneration with full-blown dementia. In this way, it may gain interest as a potential substance for the prophylaxis of the development of post-ischemic brain neurodegeneration. It is a safe substance, commercially available, inexpensive and registered as a pro-health product in the US and Europe. Taken together, the evidence available in the review on the therapeutic potential of myricetin provides helpful insight into the potential clinical utility of myricetin in treating neurodegenerative disorders with full-blown dementia. Therefore, myricetin may be a promising complementary agent in the future against the development of post-ischemic brain neurodegeneration. Indeed, there is a scientific rationale for the use of myricetin in the prevention and treatment of brain neurodegeneration caused by ischemia.
Highlights
With the aging of the world population, ischemic stroke has become the second leading cause of death in people aged 60 and over, and the fifth leading cause of death in people aged 15 to 59 worldwide [1]
Myricetin influences the increase of autophagy (Figure 1), which results in the elimination of toxic amyloid and the dysfunctional tau protein produced by neurons [102,123]
Disruption of the balance of metal ions in an ischemic brain can result in cytotoxicity, oxidative stress, increased amyloid deposition and tau protein hyperphosphorylation, changes closely related to post-ischemic brain neurodegeneration [9,10,11,14]
Summary
With the aging of the world population, ischemic stroke has become the second leading cause of death in people aged 60 and over, and the fifth leading cause of death in people aged 15 to 59 worldwide [1]. Targeting these phenomena may be an essential strategy in the treatment of post-ischemic brain neurodegeneration In this context, the use of myricetin in the treatment of ischemic neurodegeneration has certain advantages: namely, it (1) decreases the production of amyloid, (2) prevents the development of amyloid oligomers and fibrils, (3) protects the development of neurofibrillary tangles, (4) decreases neuroinflammation, (5) acts as a powerful anti-oxidant, (6) prevents metals from binding to amyloid and tau protein, (7) increases acetylcholine levels (Figure 1), and (8) can be taken in relatively high quantities without side effects [102]. Of the review, we present a possible use of myricetin in the treatment of post-ischemic brain neurodegeneration that has neuropathological changes similar to Alzheimer’s disease
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