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.

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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