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New research helps explain genetics of Parkinson's disease
November 24, 2008A 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 (www.jcb.org).
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.
Rockefeller University Press
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.
Rockefeller University Press
Mitochondria Current Events and Mitochondria News RSSHydrogen Peroxide's Link to Living Cells
If a circadian rhythm is like an orchestra - the united expression of the rhythms of millions of cells - a common chemical may serve as the conductor, or at least as the baton.
Developmental drug may help bone fractures heal after radiation exposure
A drug currently under development by the University of Pittsburgh School of Medicine may help bone fractures heal more quickly after radiation exposure, according to a study by Pitt researchers.
Chemosensitivity of cancer cells depends on their protein dependency
Two different anti-apoptotic proteins support cancer cell survival via an identical mechanism, yet differ in their sensitivity to chemotherapeutic drugs, report Brunelle et al. The study will be published online October 26, 2009 and in the November 2, 2009 print issue of the Journal of Cell Biology (JCB).
Too much of a good thing? Scientists explain cellular effects of vitamin A overdose and deficiency
If a little vitamin A is good, more must be better, right? Wrong! New research published online in the FASEB Journal shows that vitamin A plays a crucial role in energy production within cells, explaining why too much or too little has a complex negative effect on our bodies.
How mitochondrial gene defects impair respiration, other major life functions
Researchers are delving into abnormal gene function in mitochondria, structures within cells that power our lives. Mitochondria are the place where energy is generated from the most basic molecules of food. Because this function is essential to life, defects in mitochondria may affect a wide range of organ systems in humans and animals.
Can an over-the-counter vitamin-like substance slow the progression of Parkinson's disease?
Rush University Medical Center is participating in a large-scale, multi-center clinical trial in the U.S. and Canada to determine whether a vitamin-like substance, in high doses, can slow the progression of Parkinson's disease, a neurodegenerative disorder that affects about one million people in the United States.
Evolution still scientifically stable
An international team of researchers, including Monash University biochemists, has discovered evidence at the molecular level in support of one of the key tenets of Darwin's theory of evolution.
Study: Popular supplement quercetin does not enhance athletic performance
The antioxidant quercetin is increasingly being marketed as a supplement that boosts athletic performance, but a new University of Georgia study finds that it is no better than a placebo.
Gene mutation responsible for premature skin aging disease identified
In the new print issue of Nature Genetics, scientists in Singapore and Germany report that mutations in the PYCR1 gene cause the rare genetic condition that results in premature skin aging and that is known as "wrinkly skin syndrome."
Carnitine supplements reverse glucose intolerance in animals
Supplementing obese rats with the nutrient carnitine helps the animals to clear the extra sugar in their blood, something they had trouble doing on their own, researchers at Duke University Medical Center report.
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