Medical researchers conclude that simvastatin should not be used as treatment for multiple sclerosis

This study was published in Lancet Neurology 2011 Aug;10(8):691-701

Study title and authors:
Simvastatin as add-on therapy to interferon β-1a for relapsing-remitting multiple sclerosis (SIMCOMBIN study): a placebo-controlled randomised phase 4 trial.

Sorensen PS, Lycke J, Erälinna JP, Edland A, Wu X, Frederiksen JL, Oturai A, Malmeström C, Stenager E, Sellebjerg F, Sondergaard HB

Danish Multiple Sclerosis Center, Department of Neurology, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark. pss@rh.dk

This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/21742556

This study investigated the effects of statins in patients relapsing-remitting multiple sclerosis who were receiving the multiple sclerosis drug interferon beta. The three year study was a placebo-controlled, double-blind, randomised, parallel-group trial and included 307 patients who received either simvastatin or placebo.

The study found:
(a) Patients in the simvastatin group had a 39% higher risk of relapse compared to patients in the placebo group.
(b) Patients in the simvastatin group had their first relapse 3.4 months earlier than patients in the placebo group.
(c) Patients in the simvastatin group had a 17% higher risk of new or enlarging lesions compared to patients in the placebo group.
(d) Patients in the simvastatin group had a 58% reduced chance of having no disease activity compared to patients in the placebo group.

The researchers concluded: "The combination of interferon beta and simvastatin should not be used as treatment for relapsing-remitting multiple sclerosis".

Statins may be implicated in neurodegenerative diseases

This post includes a summary of a paper published in Neurobiology of Aging 2010 Sep;31(9):1543-53

Study title and authors:
Mevastatin accelerates loss of synaptic proteins and neurite degeneration in aging cortical neurons in a heme-independent manner.

Kannan M, Steinert JR, Forsythe ID, Smith AG, Chernova T.

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MRC Toxicology Unit, University of Leicester, Leicester, United Kingdom.

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/18951667

Kannan investigated the effectes of statins on cultured neurons.

The study found:
(a) Statins impaired synaptic proteins.
(b) Statins reduced N-methyl-d-aspartate receptor currents (N-methyl-d-aspartate receptor currents help in memory funcion).
(c) Statins accelerated neurodegeneration associated with aging.

To conclude: Statins exert a neurotoxic effect in cultured neurons and may be implicated in neurodegenerative diseases such as Parkinson’s, Alzheimer’s, Amyothrophic Lateral Sclerosis, Multiple Sclerosis and Huntington’s.

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Statins implicated in multiple sclerosis

This post includes a synopsis of a study published in the Journal of  Neuroscience Research 2010 Nov 15;88(15):3361-75

Study title and authors:
Simvastatin interferes with process outgrowth and branching of oligodendrocytes.
Smolders I, Smets I, Maier O, vandeVen M, Steels P, Ameloot M.
Biomedical Research Institute, School of Life Sciences, Hasselt University and Transnational University Limburg, Diepenbeek, Belgium.

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/20857509

Oligodendrocytes are a type of brain cell. They are the cell type that is predominantly affected in multiple sclerosis. Myelin is the protective sheath coating our nerve fibers.

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Any adverse effects on oligodendrocytes and myelin are detrimental and are implicated in multiple sclerosis.

The study focused on the effects of stain drugs on oligodendrocytes and myelin in a laboratory setting.

The study found:
(a) Cholesterol is required for the growth of oligodendrocytes.
(b) Statins inhibited the growth of oligodendrocytes.
(c) Statins inhibited the growth of myelin.

To conclude: Statin treatment has detrimental effects on oligodendrocyte growth, which is the prior step in (re)myelination, and thereby inhibits the healing of multiple sclerosis lesions.

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Statin use as a pathway to multiple sclerosis

This post includes a summary of a paper published in The Journal of Neuroscience December 10, 2008, 28(50):13609-13614

Study title and authors:
Negative Impact of Statins on Oligodendrocytes and Myelin Formation In Vitro and In Vivo
Steve Klopfleisch,1 * Doron Merkler,2 * Matthias Schmitz,1 Sabine Klöppner,1 Mariann Schedensack,2 Gunnar Jeserich,4 Hans H. Althaus,1 and Wolfgang Brück2,3
1Max Planck Institute for Experimental Medicine, 37075 Göttingen, Germany, 2Department of Neuropathology, University Medical Centre, Georg August University, 37075 Göttingen, Germany, 3Institute for Multiple Sclerosis Research, Gemeinnützige Hertie-Stiftung and University Medical Centre Göttingen, 37073 Göttingen, Germany, and 4Department of Neurobiology, University of Osnabrück, 49076 Osnabrück, Germany

This paper can be accessed at: http://www.jneurosci.org/cgi/content/abstract/28/50/13609

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Oligodendrocytes are a type of brain cell. Oligodendrocytes are responsible for producing a fatty protein, called myelin, which insulates axons, the long extensions of nerve cells (neurons). Myelinated axons transmit nerve signals much faster than unmyelinated ones. Each oligodendrocyte can supply myelin for several axons and each axon can be supplied by several oligodendrocytes. Oligodendrocytes wrap the myelin around the axons in thin sheets like rolled up paper.

 
This study investigated the relationship of statins and myelin formation in cultured cells and in a trial.

The study reports:
(a) Cholesterol is a major component of myelin.
(b) Statins are drugs which lower cholesterol levels.
(c) Lower cholesterol levels disrupt oligodendrocytes from producing myelin.
(d) Lack of myelin allows lesions to form on the neurons, which disrupts signals between the brain and other parts of the body leading to multiple sclerosis.

The study provides evidence that statins impair remyelination of axons by oligodendrocytes, which could lead to multiple sclerosis.
 
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