Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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, December 7, 2025

Coenzyme Q10 attenuates age-associated neurodegeneration via modulation of autophagy and neuroinflammation in aged rats

 

What does your doctor have to say about this?
Can coenzyme Q10 reduce the risk of side effects from statins?

The latest here:

Coenzyme Q10 attenuates age-associated neurodegeneration via modulation of autophagy and neuroinflammation in aged rats

Abstract

This study investigates the neuroprotective potential of Coenzyme Q10 (CoQ10) in aging rats, with emphasis on its roles in modulating autophagy and reducing inflammaging. Male Wistar rats, both young (4 months) and aged (24 months), were orally administered CoQ10 at a dose of 20 mg/kg body weight for 28 days. Biochemical analysis revealed a significant enhancement in antioxidant defenses, as evidenced by elevated ferric reducing antioxidant power (FRAP), reduced glutathione (GSH), and increased activities of superoxide dismutase (SOD) and catalase (CAT). In parallel, levels of oxidative stress biomarkers—including malondialdehyde (MDA), advanced oxidation protein products (AOPP), protein carbonyls (PCO), and nitric oxide (NO)—were significantly reduced. CoQ10 supplementation also restored mitochondrial function, as indicated by increased activities of electron transport chain complexes in the brain. Gene expression analysis via reverse transcriptase-polymerase chain reaction (RT-PCR) showed up-regulation of autophagy markers Beclin-1 and ULK-1, alongside down-regulation of pro-inflammatory cytokines IL-6 and TNF-α, suggesting a reduction in neuroinflammation. Histopathological analysis supported these findings, demonstrating improved structural integrity of brain cells in CoQ10-treated rats. Overall, these results indicate that CoQ10 exerts multifaceted neuroprotective effects through enhancement of antioxidant defenses, restoration of mitochondrial function, activation of autophagy, and suppression of inflammation, thereby offering a promising intervention to mitigate age-associated neurodegeneration.

Graphical Abstract

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