Be still my pizza heart. Now, if only cholesterol didn't literally work to stop it, sigh. - Dave
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Dietary cholesterol promotes repair of demyelinated lesions in the adult brain
Stefan A. Berghoff, Nina Gerndt, Jan Winchenbach, Sina K. Stumpf, Leon Hosang, Francesca Odoardi, Torben Ruhwedel, Carolin Böhler, Benoit Barrette, Ruth Stassart, David Liebetanz, Payam Dibaj, Wiebke Möbius, Julia M. Edgar*& Gesine Saher
Nature Communications 8, Article*number:*14241 (2017)
doi:10.1038/ncomms14241
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Multiple sclerosisOligodendrocyte
Received:
22 April 2016
Accepted:
12 December 2016
Published online:
24 January 2017
Abstract
Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure contributes to persistent disability. Cholesterol is rate-limiting for myelin biogenesis in the developing CNS; however, whether cholesterol insufficiency contributes to remyelination failure in MS, is unclear. Here, we show the relationship between cholesterol, myelination and neurological parameters in mouse models of demyelination and remyelination. In the cuprizone model, acute disease reduces serum cholesterol levels that can be restored by dietary cholesterol. Concomitant with blood-brain barrier impairment, supplemented cholesterol directly supports oligodendrocyte precursor proliferation and differentiation, and restores the balance of growth factors, creating a permissive environment for repair. This leads to attenuated axon damage, enhanced remyelination and improved motor learning. Remarkably, in experimental autoimmune encephalomyelitis, cholesterol supplementation does not exacerbate disease expression. These findings emphasize the safety of dietary cholesterol in inflammatory diseases and point to a previously unrecognized role of cholesterol in promoting repair after demyelinating episodes.
FULL ARTICLE: http://www.nature.com/articles/ncomms14241
Hence, cholesterol supplementation enhances repair after demyelination and improves neurological outcomes by supporting oligodendrocyte proliferation and differentiation, promoting remyelination, decreasing microgliosis, and attenuating axonal damage in a permissive environment (‘induced remyelination’ after cuprizone withdrawal).
Dietary cholesterol promotes repair of demyelinated lesions in the adult brain
Stefan A. Berghoff, Nina Gerndt, Jan Winchenbach, Sina K. Stumpf, Leon Hosang, Francesca Odoardi, Torben Ruhwedel, Carolin Böhler, Benoit Barrette, Ruth Stassart, David Liebetanz, Payam Dibaj, Wiebke Möbius, Julia M. Edgar*& Gesine Saher
Nature Communications 8, Article*number:*14241 (2017)
doi:10.1038/ncomms14241
Download Citation
Multiple sclerosisOligodendrocyte
Received:
22 April 2016
Accepted:
12 December 2016
Published online:
24 January 2017
Abstract
Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure contributes to persistent disability. Cholesterol is rate-limiting for myelin biogenesis in the developing CNS; however, whether cholesterol insufficiency contributes to remyelination failure in MS, is unclear. Here, we show the relationship between cholesterol, myelination and neurological parameters in mouse models of demyelination and remyelination. In the cuprizone model, acute disease reduces serum cholesterol levels that can be restored by dietary cholesterol. Concomitant with blood-brain barrier impairment, supplemented cholesterol directly supports oligodendrocyte precursor proliferation and differentiation, and restores the balance of growth factors, creating a permissive environment for repair. This leads to attenuated axon damage, enhanced remyelination and improved motor learning. Remarkably, in experimental autoimmune encephalomyelitis, cholesterol supplementation does not exacerbate disease expression. These findings emphasize the safety of dietary cholesterol in inflammatory diseases and point to a previously unrecognized role of cholesterol in promoting repair after demyelinating episodes.
FULL ARTICLE: http://www.nature.com/articles/ncomms14241
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