New research helps explain genetics of Parkinson's disease

Nov 24, 2008

A new study by Narendra et al. suggests that Parkin, the product of the Parkinson's disease-related gene Park2, prompts neuronal survival by clearing the cell of its damaged mitochondria.

"[This is] an exciting new discovery that links the fields of mitochondrial quality control and the genetics of Parkinson's disease (PD)," writes Heidi McBride of the University of Ottawa Heart Institute. "…This work significantly increases our understanding of PD and provides a new framework for the development of therapeutic interventions."

The study, as well as McBride's commentary, will appear in the December 1, 2008 print issue of the Journal of Cell Biology (JCB). Both articles will be published online Monday, November 24.

Loss-of-function mutations in the gene Park2, which encodes an E3 ubiquitin ligase (Parkin), are implicated in half the cases of recessive familial early-onset Parkinson's disease. Several lines of evidence suggest that Parkin loss is associated with mitochondrial dysfunction, but exactly how was unknown. To learn more about Parkin's role in cells, Narendra et al. examined the protein's subcellular location. They found that Parkin was present in the cytoplasm of most cells, but translocated to mitochondria in cells that had undergone mitochondrial damage such as membrane depolarization.

Damaged mitochondria can trigger cell death pathways; indeed, dysregulation of mitochondrial health was already thought to be a possible cause of the neuronal cell death associated with Parkinson's disease. The relocation of Parkin to damaged mitochondria, the team showed, sends these defunct organelles to autophagosomes for degradation. Parkin may thus prevent the damaged mitochondria from triggering cell death. Because neurons are not readily replicable, disposing of damaged mitochondria may be especially important in the adult brain.

Citation: Narendra, D., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200809125. (www.jcb.org)

Source: Rockefeller University

Explore further: NIH issues finalized policy on genomic data sharing

add to favorites email to friend print save as pdf

Related Stories

Quality control of mitochondria as a defense against disease

Jan 20, 2014

Scientists from the Montreal Neurological Institute and Hospital in Canada have discovered that two genes linked to hereditary Parkinson's disease are involved in the early-stage quality control of mitochondria. The protective ...

New insight into Parkinson's disease

Apr 19, 2010

New research provides crucial insight into the pathogenic mechanisms of Parkinson's disease (PD), a prevalent neurodegenerative disorder. The study appears in the April 19 issue of the Journal of Cell Biology.

When cells run out of fuel

Aug 24, 2009

Parkinson's disease is caused by the degeneration of neurons in the midbrain. The mechanisms leading to the loss of these neurons, however, are largely unknown. Recent research revealed that about ten per cent of cases are ...

Recommended for you

Study identifies genetic change in autism-related gene

13 hours ago

A new study from Bradley Hospital has identified a genetic change in a recently identified autism-associated gene, which may provide further insight into the causes of autism. The study, now published online in the Journal of ...

NIH issues finalized policy on genomic data sharing

Aug 27, 2014

The National Institutes of Health has issued a final NIH Genomic Data Sharing (GDS) policy to promote data sharing as a way to speed the translation of data into knowledge, products and procedures that improve health while ...

The genes behind the guardians of the airways

Aug 27, 2014

Dysfunctions in cilia, tiny hair-like structures that protrude from the surface of cells, are responsible for a number of human diseases. However the genes involved in making cilia have remained largely elusive. ...

Cancer leaves a common fingerprint on DNA

Aug 25, 2014

Regardless of their stage or type, cancers appear to share a telltale signature of widespread changes to the so-called epigenome, according to a team of researchers. In a study published online in Genome Me ...

User comments : 0