A Step Forward in Parkinson’s Disease

by Sahil Rawal (’19)

Fig. 1: The endoplasmic reticulum plays an important role in causing mitochondrial toxicity because of mitofusins which tether the two together.

Parkinson’s Disease is a very deadly condition with unknown origins, as scientists have been unable to pinpoint an exact explanation for its occurrence. Previous studies have shown that patients with Parkinson’s lack dopamine-producing cells, which causes attenuation of motor skills. Furthermore, it has been shown that mitochondrial toxicity causes mutations in PINK1 and PARKIN genes in patients with Parkinson’s. However, these ideas are now beginning to be disproved.

A study conducted by Dr. Celardo at the MRC Toxicology Unit found that mitochondrial toxicity is not the exact cause of the gene mutations. By using fruit flies to conduct this study, Cerlado found that when the endoplasmic reticulum becomes stressed, it transfers the stress to the mitochondria, which then causes the toxicity. Fruit flies that had the PINK1 and PARKIN mutation were found to have an excessive amount of endoplasmic reticulum stress. This stress affects the mitochondria because it is connected to the ER by mitofusin bridges. The mutation in the two genes causes more mitochondria to bind to the ER, which is correlated to fewer dopamine-producing cells. That said, though mitochondrial toxicity does play a role in Parkinson’s, endoplasmic reticular stress does as well.

This study is a good step forward in determining the exact cause of Parkinson’s Disease, and hopefully future research will bring us even closer.



  1. Celardo, et al., Mitofusin-mediated ER stress triggers neurodegeneration in pink1/parkin models of Parkinson’s disease. Cell Death and Disease 7, (2016). doi: 10.1038/cddis.2016.173.
  2. Image retrieved from: https://www.google.com/search?site=&tbm=isch&source=hp&biw=1440&bih=829&q=endoplasmic+reticulum&oq=endop&gs_l=img.3.0.0l10.1542.2006.0.3006.….0…1ac.1.64.img..0.5.357.d6YhqQv4mg4#imgrc=UerqEEacWYil7M%3A

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