CSF MicroRNAs Reveal Impairment of Angiogenesis and Autophagy in PD
This research report, which appears in this month's Neurology Genetics points out that a degradation of the functioning of the Blood Brain Barrier leads to the inability of the brain to rid itself of bad stuff. MiRNAs provide the evidence and explanation.
Discussion (of Clinical Trial) NCT02954978 (which my CSF participated in)
"This study suggests vascular and autophagy defects in Parkinson progression. Nilotinib 300mg reverses these effects via alteration of miRNA expression, suggesting epigenomic changes that may underlie long-term disease modifying effects." Here's a link to the report:
I plan to attend Marc Anderson's HU Zoom meeting at 11am Central time Dec 19 if you are interested in discussion. We'll also be talking about Sulforaphane test.
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"Dr. Donald Grosset, the clinical director of the UK Parkinson’s Excellence Network, told MNT: 'At the relatively advanced stage studied here, there could be a multitude of other reasons why these RNAs are altered. For example, the changes could signal the secondary effects of having Parkinson’s, rather than being the primary drivers for the disease’s progression.'”
"He added: 'Despite some doubts regarding the study’s methodology, investigating nilotinib’s role as a potential neuroprotective is incredibly significant. Overall, this study is adding significantly to our understanding about cerebrospinal fluid biomarker changes, especially relating to this type of treatment. I welcome this study’s initial findings, but much more research and clarity [are] needed in this critical area.'”
Evidently, vinpocetine is a multi-action agent with a variety of pharmacological targets. Its multi-actions, including vasodilation, anti-oxidation, anti-inflammation, anti-thrombosis, and anti-remodeling, may act together to elicit synergistic therapeutic effects, thereby providing significant benefits to those multifactorial cerebrovascular and cardiovascular diseases. In addition, vinpocetine is effective for a wide range of pathological conditions. The explanation could be that many diseases share common pathologies that can be improved by vinpocetine, such as antagonizing inflammation in a variety of cell types, protecting different cells from death during ischemia injuries, and stimulating vasodilation to increase blood flow in diverse tissues. It should be noted that recent findings aimed to explore novel functions of vinpocetine are largely dependent on animal models. Clinical studies in humans are necessary to validate the effectiveness of vinpocetine in preventing pathological vascular and cardiac remodeling as well as in various inflammatory diseases. Molecular mechanisms underlying some of pharmacological effects of vinpocetine, including metabolic enhancement, anti-oxidation and anti-thrombosis, still remain unclear and need to be further investigated. Successful development of genetic modified animals including gene knockout mice or transgenic mice of PDE1 isoforms, IKK, and the sodium channels would facilitate the elucidation of more precise mechanistic action of vinpocetine.
VPN is well absorbed from small intestine, which increased by food, therefore, fasting bioavailability is 6.7% and non-fasting bioavailability is 60–100%.
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