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.

Showing posts with label neuroprotective. Show all posts
Showing posts with label neuroprotective. Show all posts

Saturday, May 9, 2026

Dandelion leaves boost brain-protective compounds after digestion

The open area behind my condo is filled with dandelions but I'll not partake of them. I'm using coffee for that purpose.

 Dandelion leaves boost brain-protective compounds after digestion

A common wild plant may hold hidden brain benefits. Dandelion leaf polyphenols survive digestion and continue targeting pathways associated with Alzheimer’s disease. 

Dandelion. Picked fresh dandelion leaves and yellow flowers in home gardenStudy: Characterisation of Dandelion Polyphenols and Their In Vitro Neuroprotective Effects During Simulated Digestion. Image credit: DUSAN ZIDAR/Shutterstock.com

A recent study in Foods examined the enzyme-targeted neuroprotective potential of polyphenols from dandelion flowers, roots, and leaves during in vitro simulated digestion.

Pathological mechanisms and the limited therapeutics

Neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease represent one of the most pressing challenges in modern medicine. These diseases are characterized by progressive loss of neuronal structure and function, leading to irreversible cognitive and motor decline.

A central mechanism in AD pathogenesis involves the progressive loss of cholinergic neurons and the resulting decline in brain acetylcholine (ACh) levels. This process is accelerated by elevated acetylcholinesterase (AChE) activity, the enzyme that hydrolyzes ACh.

Beyond AChE, lipoxygenase (LOX) and reactive nitrogen species (RNS) are also involved. A dysregulated LOX activity promotes neuroinflammation, while RNS accumulation under oxidative stress can trigger neuronal death.

As global populations age, prevalence rates of neurodegenerative diseases are rising sharply. Despite decades of research, disease-modifying therapies remain difficult to achieve, and current pharmacological approaches largely manage symptoms rather than addressing underlying pathology. This has intensified interest in naturally derived compounds as complementary or preventive strategies.

Polyphenols are among the most biologically active plant metabolites with reported neuroprotective effects. While digestion generally reduces phenolic content, some fractions increase at specific stages and retain post-digestive enzyme-inhibitory activity, such as inhibition of AChE, highlighting their potential functional relevance after digestion and the importance of studying them in food-relevant conditions.

Assessing the neuroprotective functions of dandelion

Dandelion (Taraxacum officinale), widely used in traditional medicine, is a rich source of flavonoids and phenolic acids, making it a compelling subject for neuroprotection research. This study investigates polyphenol content, phenolic composition, and enzyme-targeted neuroprotective activity across different anatomical parts of the dandelion to assess its potential as a neuroprotective functional food ingredient.

The authors harvested and air-dried dandelions from Yuncheng, China, in March 2023. Dried flowers, roots, and leaves were ground and sieved, and polyphenols were extracted using a standard protocol. Total Polyphenol Content (TPC) and Total Flavonoid Content (TFC) were estimated. Researchers also determined and quantified individual polyphenols.The enzyme-inhibitory and antioxidant-related neuroprotective effects of dandelion polyphenols were assessed in vitro, and a simulated digestion model was used to evaluate their behavior during the oral, gastric, and intestinal phases.

Digestive bioaccessibility of dandelion leaf polyphenols drives superior neuroprotective effect

Dandelion leaves (DL) consistently yielded the richest polyphenol profile, recording the highest total phenolic content (TPC) of 3986.67 mg GAE/100 g (≈39.87 mg/g) and total flavonoid content (TFC) of 3250.00 mg RE/100 g (≈32.50 mg/g) among the three plant parts examined. Dandelion flowers (DF) ranked second, while dandelion roots (DR) contained the lowest levels of both phenolics and flavonoids.

Beyond total polyphenol content, the individual phenolic profiles differed markedly across plant parts. Protocatechuic acid and chicoric acid were most concentrated in DL, whereas rutin and caffeic acid accumulated preferentially in DF.

Ultra-performance liquid chromatography coupled with electrospray ionisation quadrupole time-of-flight mass spectrometry (UPLC-ESI-Q-TOF-MS) analysis of all three tissue extracts identified 84 compounds across four chemical subclasses, predominantly phenolic acids. In addition, caffeoylquinic acid derivatives and hydroxybenzoic acid derivatives, flavonoids comprising both free aglycones and glycosylated forms, coumarins, and a single tannin completed the profile.

Multivariate analysis using principal component analysis (PCA), partial least squares discriminant analysis (PLS-DA), and hierarchical clustering heat maps collectively revealed clear tissue-specific differences in dandelion metabolite composition. Overall, flavonoids and phenolic acids together dominated the compound class distribution in near-equal proportions (~46% each), reinforcing their central role in defining the chemical identity of each dandelion tissue.

All three dandelion tissue extracts inhibited AChE in a concentration-dependent manner, with DL consistently outperforming DF and DR, suggesting that dandelion leaf is a promising natural candidate for cholinesterase-targeted strategies in Alzheimer’s disease management. This is likely to involve non-competitive inhibition mechanisms observed with plant polyphenols.

DL showed the strongest LOX inhibitory activity, followed by DF and DR. At low concentrations, DF demonstrated markedly superior RNS scavenging over DL and DR, suggesting its phenolic composition is particularly effective against nitrogen-centred radicals.

TPC increased modestly during oral digestion, declined under gastric acidity, then increased substantially during the intestinal phase, reaching the highest levels across all samples as hydrolases and bile salts released bound phenolics.

Meanwhile, TFC peaked at the oral stage, declined under gastric conditions, and partially recovered during the intestinal phase, with DL maintaining the highest levels throughout. Across all digestion stages, DL consistently released the highest combined quantities of total phenols and flavonoids, followed by DF and DR.

Following simulated digestion, all three tissues retained measurable but generally reduced AChE-inhibitory, LOX-inhibitory, and RNS-scavenging activities. AChE inhibition was highest in the oral phase and declined progressively through gastric and intestinal stages, with reductions partly attributed to structural changes in phenolic compounds under digestive conditions and changes in interactions among phenolic constituents.

LOX inhibition was maintained or, in some cases (notably DR in the intestinal phase), enhanced, reflecting the release or activation of specific phenolics.

RNS scavenging activity remained significant across all tissues, with DF consistently showing the strongest activity, particularly at lower concentrations, while differences between tissues diminished at higher concentrations.

Conclusions

Dandelion leaves were found to be the richest source of phenols and flavonoids, with their polyphenols showing notable inhibition of enzymes involved in neurodegeneration and inflammation.

Together, these findings suggest that dandelion leaves, in particular, hold meaningful potential as a functional food ingredient for supporting neurological health and reducing the risk of conditions such as Alzheimer’s disease. Although these findings are based on in vitro enzyme assays and simulated digestion models, in vivo studies are needed to confirm these outcomes.

Download your PDF copy by clicking here.

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.

Wednesday, December 10, 2025

The Neuroprotective Effect of Garlic

 Now our stroke medical 'professionals' need to come up WITH EXACT PROTOCOLS to save as many neurons(hundreds of millions to billions!) as possible the first week when the neuronal cascade of death is occurring.

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?

The Neuroprotective Effect of Garlic

  • Chapter
  • First Online: 
Plant-Based Therapeutics, Volume 3

Saturday, September 6, 2025

Fujian tablet regulates the Foxo3a/GPX4 axis to promote remyelination and improve motor function in ischemic stroke

 Your competent? doctor KNOWS EXACTLY HOW MUCH DEMYELINATION HAS OCCURRED and has EXACT PROTOCOLS TO FIX THAT! RIGHT? NO? So your doctor knows nothing and is completely fucking incompetent? Will your doctor once again prove incompetence by not getting human testing done?
  • demyelination (10 posts to November 2013)
  • demyelinating (24 posts to May 2012)
  • myelination (8 posts to May 2016)
  • myelin-associated inhibitors (1 post to February 2017)
  • myelin-associated glycoprotein (1 post to May 2015)
  • Fujian tablet regulates the Foxo3a/GPX4 axis to promote remyelination and improve motor function in ischemic stroke


    https://doi.org/10.1016/j.jep.2025.120543Get rights and content

    Abstract

    Ethnopharmacological relevance

    Fujian Tablet (FJT), a traditional Chinese herbal compound formulation developed under the theoretical framework of “nourishing the liver and kidney, replenishing essence and marrow”, has been clinically applied for over two decades to treat post-stroke neurological deficits. Preliminary studies demonstrated its efficacy in improving motor function and promoting cervical spinal cord neuroaxonal growth in a middle cerebral artery occlusion (MCAO) rat model. Building upon these findings, this study integrates metabolomic evidence of Foxo3a-GPX4 axis activation to systematically elucidate Fujian Tablet's neurorestorative mechanisms through three interconnected pathways: regulation of ferroptosis, promotion of oligodendrocyte proliferation, and remyelination. By bridging traditional TCM therapeutic principles with contemporary molecular neuroscience, this investigation aims to provide mechanistic insights for optimizing Fujian Tablet's clinical application and advancing its global recognition in neurorehabilitation.

    Aim of the study

    This study aims to verify the molecular mechanism by which FJT activates Forkhead box O3a (Foxo3a) to promote glutathione peroxidase 4 (GPX4) expression, thereby regulating oligodendrocyte survival and remyelination, based on the regulatory network of “traditional Chinese medicine compound - target - cellular function”. This study provides experimental evidence for explaining the material basis and action targets of the compound's efficacy.

    Materials and methods

    The middle cerebral artery embolization method was employed to establish a rat model of MCAO. Then, FJT was used for intervention via intragastric administration at doses of 0.72 g/kg and 1.44 g/kg, twice daily for 14 consecutive days. Behavioral observations of the rats were carried out using the Catwalk system and beam walking test (BWT). remyelination was assessed via luxol fast blue (LFB) staining and transmission electron microscopy. In addition, in vitro experiments with oligodendrocytes were conducted in combination. The expressions of myelin basic protein (MBP) was detected by immunofluorescence. The expressions of Ferritin, and GPX4 were detected by RT-qPCR and Western blot.
    The levels of ferroptosis - related metabolites were measured using flow cytometry and enzyme - linked immunosorbent assay (ELISA). The transcriptional regulatory effect of Foxo3a on GPX4 was examined by ChIP-qPCR.

    Results

    Fujian Tablet dose-dependently improved the motor function of MCAO rats, and upregulated the expression of Foxo3a to enhance its binding activity to the GPX4 promoter, thereby increasing GPX4 expression. Knockdown of Foxo3a or treatment with the GPX4 inhibitor (RSL3) reversed the inhibitory effect of FJT on ferroptosis (decrease in lipid reactive oxygen species (ROS) and malondialdehyde (MDA), and increase in reduced glutathione (GSH)). This reversal led to a reduction in the expression of MBP and myelin oligodendrocyte glycoprotein (MOG), inhibited the level of remyelination (decrease in LFB optical density and increase in the electron microscopy G-ratio), and hindered the recovery of motor function. In vitro experiments confirmed that serum containing FJT inhibited ferroptosis through the Foxo3a-GPX4 axis, and promoted the proliferation of oligodendrocytes.

    Conclusions

    FJT exerts a neuroprotective effect by activating the Foxo3a - GPX4 axis to inhibit ferroptosis, promote the proliferation of oligodendrocytes and remyelination, and ultimately improve motor function. This study clarifies that Fujian Tablet exerts a neuroprotective effect through regulating the “ferroptosis - oligodendrocyte proliferation - remyelination” axis, providing a scientific basis for its clinical application in ethnic medicine.

    Friday, July 25, 2025

    Neuroprotective properties of transition metal dichalcogenide nanoflowers alleviate acute and chronic neurological conditions linked to mitochondrial dysfunction

     

    Of course, your competent? doctor already knew about reactive oxygen species way back in 2005, and got research initiated. NO? So you don't have a functioning stroke doctor, do you?

    Reactive oxygen species and the modulation of stroke June 2005

  • reactive oxygen species (9 posts to July 2014)
  • And now this maybe to prevent or treat Alzheimers and Parkinsons if your competent? doctor can get followup testing going

    Neuroprotective properties of transition metal dichalcogenide nanoflowers alleviate acute and chronic neurological conditions linked to mitochondrial dysfunction

    https://doi.org/10.1016/j.jbc.2025.108498
    Get rights and content
    Under a Creative Commons license
    Open access
    Mitochondrial dysfunction is an expected cause of etiology and progression in numerous human neurological pathologies, including stroke, Alzheimer's, and Parkinson's diseases. Therefore, a neuroprotective treatment is an urgent and unmet need. Transition metal dichalcogenide nanoflowers (TMD NFs) exhibit unique biological properties. However, neuroprotective properties of these nanomaterials remain poorly understood. In the current study, the biological effect of molybdenum disulfide and molybdenum diselenide TMD NFs on neurons and astrocytes was investigated. It was found that both nanomaterials lowered reactive oxygen species levels, reduced mitochondrial impairment, and increased mitochondrial biogenesis. Neuroprotective effects of both TMD NFs resulted from upregulation of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha pathway, the biological system responsible for mitochondrial biogenesis. Furthermore, administration of TMD NFs to Caenorhabditis elegans extended lifespan of the nematodes. These results indicate that TMD NFs can be used as novel neuroprotective therapeutic agents against acute and chronic neurological condition linked to mitochondrial dysfunction.