Dietary cholesterol promotes repair of demyelinated lesions in the adult brain
Berghoff SA, Gerndt N, Winchenbach J, Stumpf SK, Hosang L, Odoardi F, Ruhwedel T, Böhler C, Barrette B, Stassart R, Liebetanz D, Dibaj P, Möbius W, Edgar JM, Saher G
Nature communications · 112 citations
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- Government
- Deutsche Forschungsgemeinschaft
- Grants
- Deutsche Forschungsgemeinschaft (SA 2014/2-1)
Based on 1 listed funder(s).
Publication
- Published
- 2017-01-24 · Nat Commun · vol. 8 · issue 1 · p. 14241
- Publisher
- Nature Portfolio
- Cited
- 149 citations · more than 97% of similar papers · 5.9× the field average
- Impact
- Top 10% most cited in its field
- References
- 70 works
- Access
- Open access (journal) · CC-BY
- Research areas
- RNA Research and Splicing · Neurogenesis and neuroplasticity mechanisms · MicroRNA in disease regulation
- Keywords
- Remyelination, Multiple sclerosis, Cholesterol, Medicine, Myelin, Demyelinating disease, Experimental autoimmune encephalomyelitis, Internal medicine, Endocrinology, Central nervous system, Immunology
- MeSH
- brain, oligodendroglia, axons, cells, cultured, stem cells, animals, mice, inbred c57bl, humans, mice, multiple sclerosis, encephalomyelitis, autoimmune, experimental, disease models, animal, cuprizone, cholesterol, cholesterol, dietary, myelin proteins, cell differentiation, cell proliferation, dietary supplements, male, primary cell culture, biomarkers
15 authors
From DE, CA, GB
- Stefan A. BerghoffMax Planck Institute of Experimental Medicine
- Nina GerndtMax Planck Institute of Experimental Medicine
- Jan WinchenbachMax Planck Institute of Experimental Medicine
- Sina K. StumpfMax Planck Institute of Experimental Medicine
- Leon HosangHertie Foundation
- Francesca OdoardiHertie Foundation
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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