Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 31,822 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Sunday, July 27, 2025
Urolithin a improves Parkinson's disease-associated cognitive impairment through modulation of neuroinflammation and neuroplasticity
Your competent? doctor needs to do two things:
1. See if this would help cognitive impairment from stroke.
2. get human testing going because of your Parkinson's risk post stroke
Urolithin A alleviates dopaminergic neurodegeneration and improves cognition in the sub-acute MPTP PD mouse model
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Urolithin A alleviates neuronal injury and inflammatory responses within the hippocampal region in MPTP-treated mice
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Urolithin A rescues synaptic damage and mitigates dendritic spine loss in the hippocampus of MPTP-treated mice
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Urolithin A activates the AKT/CREB/BDNF signaling pathway in hippocampus
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Urolithin A improves cognitive function in A53T α-synuclein transgenic PD mouse model.
Abstract
Cognitive impairment is one of the most common disabling non-motor manifestations of Parkinson's disease (PD), an age-onset condition for which there are no effective therapies available to date. Urolithin A (UA) is a natural compound produced by gut bacteria from ingested ellagitannins (ETs) and ellagic acid (EA). Our previous study showed that UA ameliorates motor deficits and dopaminergic neurodegeneration in experimental models of PD. However, its effect on PD non-motor symptoms has not been elucidated. This study aims to explore the effect of UA on cognitive impairment in MPTP-induced PD mouse model as well as in transgenic mice that overexpresses human A53T mutant α-synuclein (A53T mice). Treatment with UA reversed cognitive dysfunction as measured by Morris water maze, Y maze and novel object recognition tests in both PD models. Enhanced cognition was associated with decreased neuroinflammation in the hippocampus. Additionally, UA also reduced hippocampal neuronal dendritic spine loss and synaptic damage. Further mechanistic analyses revealed that the beneficial effects of UA on cognitive impairment appears to involve the activation of the highly protective AKT/CREB/BDNF signaling pathway. Collectively, these findings strongly suggest that UA mitigates cognitive deficits in both MPTP-induced PD mouse model and A53T mice by reducing neuroinflammation and sustaining neuroplasticity. This study provides the first evidence for a potential therapeutic effect of UA on cognitive impairment in vivo, and supports further assessment for the possible use of UA as a dietary supplement to prevent cognitive deficits in PD, and related neurodegenerative diseases.
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