Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Jun 29:13:153.
doi: 10.1186/s12916-015-0394-4.

Aspirin and multiple sclerosis

Sheila Tsau  1 , Mitchell R Emerson  2 , Sharon G Lynch  3 , Steven M LeVine  4
Affiliations
Review

Aspirin and multiple sclerosis

Sheila Tsau et al. BMC Med. .

Abstract

Aspirin is widely used to lessen the risks of cardiovascular events. Some studies suggest that patients with multiple sclerosis have an increased risk for some cardiovascular events, for example, venous thromboembolism and perhaps ischemic strokes, raising the possibility that aspirin could lessen these increased risks in this population or subgroups (patients with limited mobility and/or antiphospholipid antibodies). However, aspirin causes a small increased risk of hemorrhagic stroke, which is a concern as it could potentially worsen a compromised blood-brain barrier. Aspirin has the potential to ameliorate the disease process in multiple sclerosis (for example, by limiting some components of inflammation), but aspirin also has the potential to inhibit mitochondrial complex I activity, which is already reduced in multiple sclerosis. In an experimental setting of a cerebral ischemic lesion, aspirin promoted the proliferation and/or differentiation of oligodendrocyte precursors, raising the possibility that aspirin could facilitate remyelination efforts in multiple sclerosis. Other actions by aspirin may lead to small improvements of some symptoms (for example, lessening fatigue). Here we consider potential benefits and risks of aspirin usage by patients with multiple sclerosis.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Aspirin inhibition of the synthetic pathway of prostaglandins I2, E2, and thromboxane A2. Cyclooxygenases metabolize arachidonic acid to PGH2, which in turn is converted into various prostanoids by specific enzymes. Depending on the receptors activated by these molecules, mixed physiologic effects on the vasculature and platelet reactivity occur. Aspirin irreversibly inhibits cyclooxygenase activity. COXs = cyclooxygenases; PGH2 = prostaglandin H2; PGI synthase = prostaglandin-I synthase; PGE synthases = prostaglandin-E synthases; TXA synthase = thromboxane synthase; PGI2 = prostacyclin; PGE2 = prostaglandin E2; TXA2 = thromboxane A2; IP receptor = prostacyclin receptor; EP receptors = prostaglandin E2 receptors; TP receptors = thromboxane A2 receptors
See this image and copyright information in PMC

References

    1. Karussis D. The diagnosis of multiple sclerosis and the various related demyelinating syndromes: a critical review. J Autoimmun. 2014;48–49:134–42. doi: 10.1016/j.jaut.2014.01.022. - DOI - PubMed
    1. Kutzelnigg A, Lassmann H. Pathology of multiple sclerosis and related inflammatory demyelinating diseases. Handb Clin Neurol. 2014;122:15–58. doi: 10.1016/B978-0-444-52001-2.00002-9. - DOI - PubMed
    1. Neumann H. Molecular mechanisms of axonal damage in inflammatory central nervous system diseases. Curr Opin Neurol. 2003;16:267–73. doi: 10.1097/00019052-200306000-00004. - DOI - PubMed
    1. Lassmann H. Axonal and neuronal pathology in multiple sclerosis: what have we learnt from animal models. Exp Neurol. 2010;225:2–8. doi: 10.1016/j.expneurol.2009.10.009. - DOI - PubMed
    1. Correale J. The role of microglial activation in disease progression. Mult Scler. 2014;20:1288–95. doi: 10.1177/1352458514533230. - DOI - PubMed

Publication types

MeSH terms