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 Coenzyme Q10. Show all posts
Showing posts with label Coenzyme Q10. Show all posts

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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Wednesday, November 12, 2025

Coenzyme Q10 Modulates BDNF and it is Regulating Non-coding RNAs to Attenuate Motor Deficits and Neurodegeneration in Cerebellum of Cuprizone-Induced Demyelination Rat Model Research Published: 09 November 2025

 

 Does your competent? doctor have the correct levels for stroke recovery? Oh, your doctor doesn't even know of the need? Let's see how long your doctor has been incompetent, over a decade, WOW! And your doctor won't get human testing going?

  • BDNF (188 posts to April 2011)
  • Coenzyme Q10 Modulates BDNF and it is Regulating Non-coding RNAs to Attenuate Motor Deficits and Neurodegeneration in Cerebellum of Cuprizone-Induced Demyelination Rat Model

    Abstract

    Multiple sclerosis (MS) is a progressive neurodegenerative disorder. Limited data exist regarding the molecular mechanisms underlying cerebellar involvement and the potential role of Coenzyme Q10 (CoQ10) in non-coding RNAs in MS. This study aimed to investigate the effects of CoQ10 on histomorphometric changes, motor behaviors, and the expression of BDNF and its regulatory ncRNA in the cerebellar tissue of a rat model of demyelination. The study included four groups: control, Q10 alone, cuprizone-induced demyelination (DM), and DM + Q10 (n = 6 rats/group). Demyelination was induced by administering 0.5% cuprizone mixed in rodent chow for 12 weeks. CoQ10 (200 mg/kg/day) was given by oral gavage, dissolved in 1% sodium carboxymethyl cellulose. Behavioral tests (rotarod, open field, and inverted grid) were conducted to assess motor function. Histological analysis and molecular evaluations were conducted to assess BDNF protein levels and the expression of MALAT1, HOTAIR (HOX Transcript Antisense RNA), and phosphorylated CREB (P-CREB). The results indicated that, compared to the control group, the MS group exhibited reduced motor activity, along with histological alterations in cerebellar Purkinje cells, including decreased cell number and increased pyknosis. Molecular analyses showed a marked upregulation of non-coding RNAs MALAT1 and HOTAIR, alongside significant downregulation in the protein expression levels of BDNF and phosphorylated CREB (P-CREB). Treatment with CoQ10 notably ameliorated these histological changes by improving motor performance, restoring Purkinje cell integrity, reducing the expression of MALAT1 and HOTAIR, and enhancing the levels of BDNF and P-CREB in the cerebellum. Our results indicated that CoQ10, by modulating BDNF signaling and its regulatory non-coding RNAs, effectively counteracted molecular and cellular damage in the cerebellum, improving motor performance. This study provides new insight into the role of CoQ10 in cerebellar protection, an area that has received limited attention in demyelinating disease research.

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    Wednesday, July 17, 2024

    The Role of Coenzyme Q10 in Cardiovascular Disease Treatment: An Updated 2024 Systematic Review and Meta-Analysis of Prospective Cohort Studies (2000-2023)

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

    The latest here:

     The Role of Coenzyme Q10 in Cardiovascular Disease Treatment: An Updated 2024 Systematic Review and Meta-Analysis of Prospective Cohort Studies (2000-2023)

    Julian Yin Vieira Borges

    Abstract 

    Background: 
     
    Cardiovascular diseases (CVDs) are the leading cause of death globally. Mitochondrial dysfunction is implicated in the pathogenesis of various CVDs. Coenzyme Q10 (CoQ10), a crucial component of the mitochondrial electron transport chain, has potential cardioprotective effects. This study aims to evaluate the efficacy of adding CoQ10 nutrient supplementation in the Treatment of Cardiovascular Disease Protocols in patients with CVDs. 
     
    Methods: 
     
    This systematic review and meta-analysis assessed data from PubMed, Scopus, and Cochrane Library databases up to January 2024. Prespecified inclusion criteria were randomized controlled trials (RCTs) involving adult patients with CVDs, comparing CoQ10 supplementation with placebo or standard care. Exclusion criteria included non-randomized studies, studies without a control group, and those not reporting relevant outcomes. Data extraction and quality assessment were performed independently by two reviewers. The primary outcome was improvement in mitochondrial function, assessed through ATP production and mitochondrial respiratory capacity. Secondary outcomes included changes in systolic function, measured by ejection fraction. Statistical analysis was conducted using Review Manager software. 
     
    Findings: 
     
    The search identified 243 studies, of which 5 RCTs met the inclusion criteria, encompassing a total of 1,200 participants (600 male, 600 female). CoQ10 supplementation significantly improved mitochondrial function in cardiomyocytes, evidenced by increased ATP production and enhanced mitochondrial respiratory capacity. Additionally, CoQ10 was associated with a significant improvement in systolic function, measured by ejection fraction (mean difference: 5.6%, 95% CI: 3.2% to 8.0%, p<0.001). The risk of bias across studies was generally low, with an I statistic of 25% indicating low heterogeneity. Interpretation: This meta-analysis supports the beneficial effects of CoQ10 on mitochondrial function and systolic performance in patients with CVD. These findings suggest that CoQ10 supplementation could be a valuable adjunctive therapy in this population. However, further large-scale RCTs are necessary to confirm these results and determine the optimal dosage and duration of therapy. 
     
    Keywords: Coenzyme Q10, Ubiquinone, Cardiovascular diseases, Heart failure, Myocardial infarction,
    Coronary artery disease, Mitochondrial dysfunction, Ejection fraction, Endothelial function
    Cardiovascular Disease
    Cardiology

    Sunday, December 25, 2022

    Micronutrient Supplementation to Reduce Cardiovascular Risk

    Ask your doctor which supplements to take. Be careful of beta-carotene.  Your doctor should know if coenzyme Q10 cancels out the beta carotene risk.

    Micronutrient Supplementation to Reduce Cardiovascular Risk

    https://doi.org/10.1016/j.jacc.2022.09.048Get rights and content

    Abstract

    Background

    Healthy dietary patterns are rich in micronutrients, but their influence on cardiovascular disease (CVD) risks has not been systematically quantified.

    Objectives

    The goal of this study was to provide a comprehensive and most up-to-date evidence-based map that systematically quantifies the impact of micronutrients on CVD outcomes.

    Methods

    This study comprised a systematic review and meta-analysis of randomized controlled intervention trials of micronutrients on CVD risk factors and clinical events.

    Results

    A total of 884 randomized controlled intervention trials evaluating 27 types of micronutrients among 883,627 participants (4,895,544 person-years) were identified. Supplementation with n-3 fatty acid, n-6 fatty acid, l-arginine, l-citrulline, folic acid, vitamin D, magnesium, zinc, α-lipoic acid, coenzyme Q10, melatonin, catechin, curcumin, flavanol, genistein, and quercetin showed moderate- to high-quality evidence for reducing CVD risk factors. Specifically, n-3 fatty acid supplementation decreased CVD mortality (relative risk [RR]: 0.93; 95% CI: 0.88-0.97), myocardial infarction (RR: 0.85; 95% CI: 0.78-0.92), and coronary heart disease events (RR: 0.86; 95% CI: 0.80-0.93). Folic acid supplementation decreased stroke risk (RR: 0.84; 95% CI: 0.72-0.97), and coenzyme Q10 supplementation decreased all-cause mortality events (RR: 0.68; 95% CI: 0.49-0.94). Vitamin C, vitamin D, vitamin E, and selenium showed no effect on CVD or type 2 diabetes risk. β-carotene supplementation increased all-cause mortality (RR: 1.10; 95% CI: 1.05-1.15), CVD mortality events (RR: 1.12; 95% CI: 1.06-1.18), and stroke risk (RR: 1.09; 95% CI: 1.01-1.17).

    Conclusions

    Supplementation of some but not all micronutrients may benefit cardiometabolic health. This study highlights the importance of micronutrient diversity and the balance of benefits and risks to promote and maintain cardiovascular health in diverse populations. (Antioxidant Supplementation in the Prevention and Treatment of Cardiovascular Diseases; CRD42022315165)

    Tuesday, May 1, 2018

    At Last! A Vitamin That Can Make Your Blood Vessels Younger

    Your doctor won't know the answer but ask anyway. Which intervention causes the arteries to be the most flexible and what is the protocol to accomplish that? An extremely simple question, why the hell doesn't your doctor know the answer?

    Watermelon juice reverses hardening of the arteries Nov. 2011


    Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation June 2004

    Good News: Coffee Could Be Cleaning Out Your Arteries.  March 2018

    New study shows aged garlic extract can reduce dangerous plaque buildup in arteries Jan. 2016

    The latest one here. Did your doctor prescribe ANY of these earlier ones? Don't try any of these on your own. 

    The latest here:

    At Last! A Vitamin That Can Make Your Blood Vessels Younger



    Heart disease in all its forms continues to be the top killer of Americans. Following a heart-healthy diet like this one and getting plenty of exercise can help, but health experts continue to search for even more effective treatment—and they may have found one: A new study suggests that an antioxidant can breathe new life into old and stiff arteries.
    In the small study—published in the journal Hypertension—researchers from the University of Colorado Boulder gave ten volunteers between the ages of 60 and 79 a daily supplement called MitoQ (it's a refined version of the natural antioxidant coenzyme Q10); another ten got a placebo. After six weeks, the researchers analyzed the health and size of participants' arteries, then switched the supplement group to the placebo while the others began taking MitoQ.
    At the conclusion of their testing, researchers noted when volunteers got the supplement, their arteries regained flexibility. Essentially, MitoQ seemed to reverse artery aging by as much as 15 to 20 years. The study's lead author, post-doctoral student Matthew Rossman said in a press release that "An improvement of that magnitude, if sustained, is associated with about a 13 percent reduction in heart disease." (These are the 5 types of heart disease and their warning signs.)
    According to Rossman's co-author Doug Seals, PhD, the study "breathes new life into the discredited theory that supplementing the diet with antioxidants can improve health." He went on to note that "it suggests that targeting... mitochondria may be a better way to reduce oxidative stress and improve cardiovascular health with aging."
    Both Rossman and Dr. Seals plan to conduct additional follow-up studies to confirm their findings. Dr. Seals noted that physical activity and proper eating habits continue to be the best ways of avoiding heart disease. "At the public health level, not enough people are willing to do that," he said. "We're looking for complementary, evidence-based options to prevent age-related changes that drive disease. These supplements may be among them."

    Tuesday, April 24, 2018

    Nutraceuticals could play an important role in preventing heart disease

    This would seem to be essential to immediately help your recovery by delivering more blood and relax your arteries. But nothing will occur because your doctor and stroke hospital will do nothing because they never read and translate research into interventions. You're screwed.
    https://www.news-medical.net/news/20180420/Nutraceuticals-could-play-an-important-role-in-preventing-heart-disease.aspx
    Older adults who take a novel antioxidant that specifically targets cellular powerhouses, or mitochondria, see age-related vascular changes reverse by the equivalent of 15 to 20 years within six weeks, according to new University of Colorado Boulder research.
    The study, published this week in the American Heart Association journal Hypertension, adds to a growing body of evidence suggesting pharmaceutical-grade nutritional supplements, or nutraceuticals, could play an important role in preventing heart disease-the nation's No. 1 killer. It also resurrects the notion that oral antioxidants, which have been broadly dismissed as ineffective in recent years, could reap measurable health benefits if properly targeted, the authors say.
    "This is the first clinical trial to assess the impact of a mitochondrial-specific antioxidant on vascular function in humans," said lead author Matthew Rossman, a postdoctoral researcher in the department of integrative physiology. "It suggests that therapies like this may hold real promise for reducing the risk of age-related cardiovascular disease."
    For the study, Rossman and senior author Doug Seals, director of the Integrative Physiology of Aging Laboratory, recruited 20 healthy men and women age 60 to 79 from the Boulder area.
    Half took 20 milligrams per day of a supplement called MitoQ, made by chemically altering the naturally-occurring antioxidant Coenzyme Q10 to make it cling to mitochondria inside cells.
    The other half took a placebo.
    After six weeks, researchers assessed how well the lining of blood vessels, or the endothelium, functioned, by measuring how much subjects' arteries dilated with increased blood flow.
    Then, after a two-week "wash out" period of taking nothing, the two groups switched, with the placebo group taking the supplement, and vice versa. The tests were repeated.
    The researchers found that when taking the supplement, dilation of subjects' arteries improved by 42 percent, making their blood vessels, at least by that measure, look like those of someone 15 to 20 years younger. An improvement of that magnitude, if sustained, is associated with about a 13 percent reduction in heart disease, Rossman said. The study also showed that the improvement in dilation was due to a reduction in oxidative stress.
    In participants who, under placebo conditions, had stiffer arteries, supplementation was associated with reduced stiffness.
    Blood vessels grow stiff with age largely as a result of oxidative stress, the excess production of metabolic byproducts called free radicals which can damage the endothelium and impair its function. During youth, bodies produce enough antioxidants to quench those free radicals. But with age, the balance tips, as mitochondria and other cellular processes produce excess free radicals and the body's antioxidant defenses can't keep up, Rossman said.
    Oral antioxidant supplements like vitamin C and vitamin E fell out of favor after studies showed them to be ineffective.
    "This study breathes new life into the discredited theory that supplementing the diet with antioxidants can improve health," said Seals. "It suggests that targeting a specific source-mitochondria-may be a better way to reduce oxidative stress and improve cardiovascular health with aging."
    The study was funded by the National Institutes of Health. MitoQ Limited provided supplements and some financial support.
    This summer, Rossman and Seals plan to launch a three-month follow-up study to confirm the findings in a larger number of subjects and look more closely at the impact the compound has on mitochondria.
    The same lab published another study recently, showing that a compound called nicotinamide riboside may also be able to reverse vascular aging in healthy subjects.
    "Exercise and eating a healthy diet are the most well-established approaches for maintaining cardiovascular health," said Seals. "But at the public health level, not enough people are willing to do that. We're looking for complementary, evidence-based options to prevent age-related changes that drive disease. These supplements may be among them."