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N Engl J Med. IgG1 humanized mouse mE8-IgG2a. Minocycline-mediated inhibition of microglia activation impairs oligodendrocyte progenitor cell responses and remyelination in a non-immune model of demyelination. The clearance pathway largely depends upon astrocyte-specific water channels AQP4; efficiency of this mechanism decreases with age, with an increase in AQP4 depolarization [ , ]. Remyelination in the CNS:

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Choose your preferred view mode Please select whether you prefer to view the MDPI pages with a view tailored for mobile displays or to view the MDPI pages in the normal scrollable desktop version. This selection will be stored into your cookies and used automatically in next visits. You can also change the view style at any point from the main header when using the pages with your mobile device.

Use mobile version Use desktop version. You seem to have javascript disabled. Please note that many of the page functionalities won't work as expected without javascript enabled. Volume 8, Issue 9. No citations found yet 0. Create a SciFeed alert for new publications With following keywords neuroregeneration. By following authors Rashad Hussain.

One email with all search results. One email for each search. Open Access This article is freely available re-usable Brain Sci.

Myelin regeneration is a main therapeutic aspiration in demyelinating diseases, and the inadequacy to remyelinate rapidly has profound consequences for the health of axons and for intellectual function.

Still, there is no unwasteful treatment on stimulating myelin repair, and current therapies are circumscribed to anti-inflammatory agents. Males are lacking likely to develop multiple sclerosis than females, but often be dressed a more severe infirmity course and reach inability milestones at an earlier age than females, and these observations have spurred interest in the quiescent protective effects of androgens. Here, we demonstrate that testosterone treatment efficiently stimulates the development of original myelin and reverses myelin damage in chronic demyelinated brain lesions, resulting from the long-term administration of cuprizone, which is toxic for oligodendrocytes.

In besides to the strong significance of testosterone on myelin repair, the number of activated astrocytes and microglial cells returned to inferior control levels, indicating a reduction of neuroinflammatory responses. We likewise identify the neural androgen receptor as a novella therapeutic objective for myelin recovery. Testosterone treatment along with failed to promote remyelination after inveterate cuprizone-induced demyelination in mice with a non-functional androgen receptor.

Importantly, testosterone did not fire the founding of supplementary myelin sheaths after peculiar knockout of the androgen receptor in neurons and macroglial cells. Thus, the neural brains androgen receptor is right for the remyelination capacity of testosterone, whereas the presence of the receptor in microglia and in peripheral tissues is not sufficient to enhance remyelination. These proof establish the efficacy of androgens as remyelinating agents and modify the knowledge androgen receptor as a promising cure target seeing that remyelination treatment, thus providing the preclinical rationale on a best-seller therapeutic manoeuvre of androgens in males with multiple sclerosis.

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