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July 30, 2013; 81 (5) Editorial

Holding on to statins in Parkinson disease

Eng-King Tan, Louis C.S. Tan
First published July 24, 2013, DOI: https://doi.org/10.1212/WNL.0b013e31829d87bb
Eng-King Tan
From the Department of Neurology (E.-K.T.), Singapore General Hospital, Tan Tock Seng Hospital, National Neuroscience Institute; and Duke NUS Graduate Medical School (E.K.-T., L.C.S.T.), Singapore.
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Louis C.S. Tan
From the Department of Neurology (E.-K.T.), Singapore General Hospital, Tan Tock Seng Hospital, National Neuroscience Institute; and Duke NUS Graduate Medical School (E.K.-T., L.C.S.T.), Singapore.
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Holding on to statins in Parkinson disease
Eng-King Tan, Louis C.S. Tan
Neurology Jul 2013, 81 (5) 406-407; DOI: 10.1212/WNL.0b013e31829d87bb

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Statins, among the most widely used drugs worldwide, lower cholesterol by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase.1 While they are effective in the treatment of hyperlipidemia, their use has been linked with many neurologic diseases, such as Parkinson disease (PD; with reduced risk generally) and multiple sclerosis, primarily due to their anti-inflammatory and potential antioxidative effects.2 Atorvastatin and simvastatin are among the most frequently prescribed statins; newer ones include rosuvastatin and pravastatin. Their ability to cross the blood–brain barrier may be influenced by their lipophilicity, with lipophilic agents like simvastatin crossing the barrier better than hydrophilic ones such as pravastatin.

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  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.

  • See page 410

  • © 2013 American Academy of Neurology
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Letters: Rapid online correspondence

  • Statins, cholesterol and Parkinson disease
    • Luca Mascitelli, Medical Officer, Comando Brigata alpina Julia, Udine, Italylumasci@libero.it
    • Luca Mascitelli, Udine, Italy; Mark R Goldstein, Naples, FL
    Submitted August 06, 2013
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