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Laurance Johnston, Ph.D.


A cholesterol-lowering medicine belonging to the statin-drug group, Lipitor (tradename for atorvastatin) is one of societyís most widely used and profitable drugs. By inhibiting the liverís enzymatic production of a cholesterol precursor, it lowers cholesterol levels.  Animal and clinical studies suggest that Lipitor (or related statins) exerts a neuroprotective and anti-inflammatory influence for various neurological disorders, including MS, AD, stroke, and SCI.

Drs. Avtar and Inderjit Singh and colleagues at the Medical University of South Carolina have carried out several studies indicating that Lipitor minimizes neurological damage in rats with an experimental contusion injury (i.e., comparable to the sort of injury observed in most humans).  In the first, rats treated before and after injury with Lipitor recovered more hind-limb function than control animals (J Neurosci Res. 79(3), 2005). 

A more recent study showed that this neuroprotective effect was also observed when the rats were given Lipitor only after injury, a finding, of course, needed if the drug is to have any real-world applicability (J Neurochem; 101, 2007). Specifically, rats were given oral doses of Lipitor two, four, or six hours after injury followed thereafter by a once daily dose. Compared to controls, Lipitor-treated rats regained considerable recovery in hind-limb function, with the earlier treated rats regaining the most.

Apparently, Lipitor preserves the blood-spinal-cord barrier after injury, which, in turn, limits the infusion into the injury site of inflammatory molecules that cause function-compromising secondary damage. Overall, there was more tissue sparing in Lipitor-treated rats, including 1) less degeneration of neuronal axons, 2) degradation of the conduction-promoting, axon-insulating myelin sheath,  3) scar-forming gliosis (the production of a dense complex of neuronal support cells called glia in the injury area), and 4) apoptotic cell death. 

Lipitor also suppresses the injury-induced expression of Rho, a molecule that inhibits axonal growth and regeneration, and initiates a physiological cascade that results in the death of nearby neuronal cells.


bulletDr. Timothy Vollmer et al (Phoenix, AZ) showed that the cholesterol-lowering statin Zocor reduced lesions in subjects with relapsing-remitting MS (Lancet 363, 2004).


bulletDr. A.S. Paintlia and colleagues (Charleston, SC) showed that the cholesterol-lowering lovastatin fostered conduction-promoting, remyelination in a MS animal model (FASEB J, 19(11), 2005).


bulletDr. Scott Zamvil and associates (San Francisco, California) showed that Lipitor in combination with the MS-drug Copaxone was more effective in reversing or preventing disease in a MS animal model than either drug alone (J Clin Invest, 116(4), 2006).


bulletNIH has funded a multi-center clinical study (San Francisco, California) looking at Lipitorís ability to decrease progression from early, predictive symptoms to actual MS (


bulletUniversity of North Carolina investigators are evaluating Lipitorís potential to enhance the efficacy of the MS drug Rebif in 30 subjects with MS-predictive clinical symptoms (