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, March 15, 2026

Ginsenoside Rg2 Delays Brain Aging via Inhibiting α-Synuclein Expression and Promoting FoxO-Mediated Neurogenesis in Mice

 Will your competent? doctor ensure human testing occurs to recover your 5 lost years of brain cognition due to your stroke? Oh, your doctor doesn't consider that part of the job! Why hasn't that doctor been fired yet?

Ginsenoside Rg2 Delays Brain Aging via Inhibiting α-Synuclein Expression and Promoting FoxO-Mediated Neurogenesis in Mice

Ethnopharmacological relevance

Panax ginseng C.A. Meyer (ginseng) has been utilized in East Asian medicine for centuries to enhance cognitive function, improve memory, and mitigate age-related decline. Ginsenoside Rg2, a key bioactive saponin from red ginseng, is thought to contribute to its neuroprotective effects on brain health.

Aim of the study

This study aimed to investigate the role of α-synuclein (α-Syn) in brain aging and to elucidate whether ginsenoside Rg2 can delay brain aging by modulating α-Syn expression and promoting FoxO1-mediated neurogenesis in mice.

Materials and methods

Naturally aging mice and D-galactose-induced aging mouse models were utilized. α-Syn expression was bi-directionally manipulated in the dentate gyrus (DG) through stereotaxic injection of adeno-associated virus (AAV) for α-Syn overexpression or knockdown. Behavioral tests, immunofluorescence, Western blot, and ELISA were performed to evaluate cognitive function, neurogenesis markers (Ki67, Nestin), aging markers (p53, p21), oxidative stress indicators (MDA, LDH, CAT), and α-Syn expression. Ginsenoside Rg2 was administered to assess its effects.

Results

α-Syn expression was significantly elevated in the DG of both naturally aging and D-galactose-induced aging mice. Overexpression of α-Syn accelerated brain aging and cognitive decline, whereas knockdown alleviated these effects. Mechanistically, α-Syn overexpression inhibited neurogenesis in the DG via the FoxO1 signaling pathway. Treatment with ginsenoside Rg2 significantly reduced α-Syn expression, decreased oxidative stress and aging markers, enhanced neurogenesis, and improved cognitive function in aging mice.

Conclusions

This study demonstrates that α-Syn acts as an “accelerator” of brain aging by impairing FoxO1-mediated neurogenesis in the DG. Ginsenoside Rg2 mitigates brain aging and cognitive decline by inhibiting α-Syn expression and promoting neurogenesis, supporting the traditional use of ginseng for cognitive health and aging resilience.
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