Affiliations: [a] Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA, USA
| [b] Department of Neurology, David Geffen School of Medicine, Los Angeles, CA, USA
| [c] Department of Environmental Health, UCLA Fielding School of Public Health, Los Angeles, CA, USA
| [d] Department of Human Genetics, David Geffen School of Medicine, Los Angeles, CA, USA
Correspondence:
[*]
Correspondence to: Beate R. Ritz, MD, PhD, UCLA Fielding School of Public Health, 650 Charles Young Drive, South, Los Angeles, CA, USA. Tel.: +1 310 206 7458; E-mail: [email protected].
Abstract: This commentary discusses the strengths and limitations of utilizing the Mendelian randomization (MR) approach in Parkinson’s disease (PD) studies. Epidemiologists proposed to employ MR when genetic instruments are available that represent reliable proxies for modifiable lifelong exposures which elude easy measurement in studies of late onset diseases like PD. Here, we are using smoking as an example. The great promise of the MR approach is its resilience to confounding and reverse causation. Nevertheless, the approach has some drawbacks such as being liable to selection- and survival-bias, it makes some strong assumptions about the genetic instruments employed, and requires very large sample sizes. When interpreted carefully and put into the context of other studies that take both genetics and the environment into consideration, MR studies help us to not only ask interesting questions but also can support causal inference and provide novel insights.
