Statins may protect against Parkinson’s disease
Discontinuation of lipophilic statins may increase the risk for Parkinson’s disease, according to findings from a population-based study in Taiwan. The association was especially strong in women and the elderly.
Jou-Wei Lin, MD, PhD, and colleagues investigated whether statins could play a role in decreasing the progression of Parkinson’s disease. The researchers analyzed Taiwan’s Longitudinal Health Insurance Database 2005 and found 43,810 adults aged 50 to 99 years who did not have Parkinson’s disease and initiated statin treatment from January 2001 to December 2008. The reimbursement policy for Taiwan’s national health insurance program requests that physicians cease prescribing statins once a patient’s cholesterol has reached the treatment goal.
“This policy allowed us to see whether there was any difference in the risk of Parkinson’s [disease] in people who stopped taking statins compared to the ones who kept taking them,” Lin, a cardiologist at National Taiwan University Hospital in Taipei, said in a press release.
The primary outcome of interest was hospital or outpatient diagnosis of Parkinson’s disease by a neurologist. Participants who were diagnosed with dementia or other cerebrovascular diseases at or 1 year before index date were excluded.
Among lipophilic statin users, the incidence rate for Parkinson’s disease was 1.68 per 1 million person-days (95% CI, 1.02-2.34). Among hydrophilic statin users, the incidence rate was 3.52 per 1 million person-days (95% CI, 1.67-5.36). Treatment continuation with lipophilic statins was associated with a lower risk for Parkinson’s disease compared with discontinuation (HR=0.42; 95% CI, 0.27-0.64).
Of the lipophilic statins studied, the strongest associations with Parkinson’s disease were observed for simvastatin (HR=0.23; 95% CI, 0.07-0.73) and atorvastatin (HR=0.33; 95% CI, 0.17-0.65). The association was strong in women who used simvastatin (HR=0.11; 95% CI, 0.02-0.8) and atorvastatin (HR=0.24; 95% CI, 0.09-0.64), as well as in those aged older than 65 years who used atorvastatin (HR=0.42; 95% CI, 0.21-0.87).
There was no association between Parkinson’s disease and continuation or discontinuation of hydrophilic statins.
“Due to the amphiphilic side chain in their molecular structures, lipophilic statins are able to cross the blood-brain barrier more readily than hydrophilic statins,” Lin and colleagues wrote. “These good penetration abilities into the neuronal and glial cells could be associated with more antioxidant and anti-inflammatory effects than the hydrophilic statins.”
In a related editorial, Eng-King Tan, MD, and Louis C.S. Tan, MD, both from Duke-National University of Singapore Graduate Medical School, said the study captured valuable data, but it may not have adequately accounted for modulatory effects such as smoking, caffeine intake and other factors.
“While there is some consensus that lipophilic statins can easily cross the blood-brain barrier and are likely to have a direct neuroprotective effect, the possibility of an indirect effect through changes in cholesterol or other lipids cannot be discounted,” they wrote.
According to the authors, the study could be a basis for further research into why statins may inhibit the onset of Parkinson’s disease.
“While there is a biological basis for the association between statin use and [Parkinson’s disease], more research is required to further decipher the specific pathways or targets that are involved in statin-induced neuroprotection. As statins inhibit the enzyme that regulates the synthesis of cholesterol from mevalonic acid, identifying the exact role of cholesterol and isoprenoids in the mevalonate pathway could provide vital clues,” they wrote.
For more information:
Disclosure: Eng-King Tan, MD, reports financial ties with GlaxoSmithKline, Lundbeck Pharmaceuticals and Novartis. Louis C.S. Tan, MD, and the researchers report no relevant financial disclosures.