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?
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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