Forum for Science, Industry and Business

Sponsored by:     3M 
Search our Site:

 

When cells run out of fuel

25.08.2009
Parkinson's genes ensure the energy supply of neurons

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 caused by defects in so-called Parkinson-associated genes.

Furthermore, mitochondria, the cellular powerhouses, seem to play a major role. New results from researchers at the LMU Munich under the lead of associate professor Dr. Konstanze Winklhofer and Professor Christian Haass connect both phenomena, showing that two Parkinson genes maintain the function of mitochondria. "Diseases like Parkinson's where at least some cases are unambiguously related to the dysfunction of specific genes offer a promising research opportunity," explains biochemist Dr. Konstanze Winklhofer "When we understand the function of these genes, we can learn a lot about the causes of the disease, its progress and possible new therapies." Professor Wolfgang Wurst and his group of the Institute for Developmental Genetics at the Helmholtz Center Munich also contributed to this work. (Journal of Biological Chemistry, 21 August, 2009)

Four million individuals are estimated to suffer from Parkinson's disease worldwide. This neurodegenerative disorder is characterized by rigid muscles, uncontrollable tremor and slowing – or even loss of – voluntary movements. It is caused by the death of nerve cells in a midbrain area called substantia nigra. These neurons secrete dopamine, a neurotransmitter involved in the control of movements. Thus, a loss of dopamine-producing neurons causes a dysbalance in the regulation of movements.

"Functionally impaired mitochondria have been recognized to trigger Parkinson's disease already in the early eighties," Dr. Konstanze Winklhofer says, an associate professor at the Adolf-Butenandt Institute of the Ludwig-Maximilians-Universität (LMU) in Munich. At this time it was discovered by accident that mitochondrial toxins can induce Parkinson's disease. The relevance of mitochondria to the loss of neurons seems plausible – after all, mitochondria supply the cells with energy in form of adenosine triphosphate and play a substantial role in the regulation of cell death.

The scientists' results now combine both observations on a genetic basis. They found that the Parkinson-associated genes PINK1 and Parkin functionally interact to maintain mitochondrial function. Loss of Parkin or PINK1 function impairs the morphology and activity of mitochondria, which then produce less adenosine triphosphate. "Our results also confirm the high neuroprotective potential of Parkin", Winklhofer says. "We observed that Parkin can compensate a loss of PINK1 function, but not the other way round". Winklhofer and her colleagues have shown earlier that Parkin can protect neurons under various stress conditions.

Until today, there is no possibility to prevent or cure Parkinson's disease. All pharmacological approaches are merely symptomatic and aim at replacing the neurotransmitter dopamine. Insight into the function of Parkinson-associated genes can help to identify new targets for therapeutic strategies in order to prevent or halt the loss of dopamine-producing neurons. So far, six Parkinson-associated genes are known whose functions remain to be elucidated in detail. In the case of Parkin and PINK1 scientists have made significant steps forward and now aim at uncovering the molecular mechanisms of their functions.

Publication: "Loss of parkin or PINK1 function increases DRP1-independent mitochondrial fragmentation"
Lutz, A.K., Exner, N., Fett, M.E., Schlehe, J.S., Kloos, K., Laemmermann, K., Brunner, B., Kurz-Drechsler, A., Vogel, F., Reichert, A.S., Bouman, L., Vogt-Weisenhorn, D., Wurst, W., Tatzelt, J., Haass, C., and Winkelhofer, K.F.

Journal of Biological Chemistry, 21. August 2009. Vol. 284, Issue 34, 22938-22951

Contact:
Priv.-Doz. Dr. Konstanze F. Winklhofer, M.D., Ph.D.
Adolf-Butenandt-Institute of Physiological Chemistry, Molecular Biology and Metabolic Biochemistry
Tel.: +49 (0) 89 / 2180 - 75483
Fax: +49 (0) 89 / 2180 - 75415
E-Mail: konstanze.winklhofer@med.uni-muenchen.de

Dr. Konstanze F. Winklhofer | EurekAlert!
Further information:
http://www.uni-muenchen.de
http://www.biochemie.abi.med.uni-muenchen.de/research/nbc/index.html

More articles from Life Sciences:

nachricht Staying in Shape
16.08.2018 | Max-Planck-Institut für molekulare Zellbiologie und Genetik

nachricht Chips, light and coding moves the front line in beating bacteria
16.08.2018 | Okinawa Institute of Science and Technology (OIST) Graduate University

All articles from Life Sciences >>>

The most recent press releases about innovation >>>

Die letzten 5 Focus-News des innovations-reports im Überblick:

Im Focus: Unraveling the nature of 'whistlers' from space in the lab

A new study sheds light on how ultralow frequency radio waves and plasmas interact

Scientists at the University of California, Los Angeles present new research on a curious cosmic phenomenon known as "whistlers" -- very low frequency packets...

Im Focus: New interactive machine learning tool makes car designs more aerodynamic

Scientists develop first tool to use machine learning methods to compute flow around interactively designable 3D objects. Tool will be presented at this year’s prestigious SIGGRAPH conference.

When engineers or designers want to test the aerodynamic properties of the newly designed shape of a car, airplane, or other object, they would normally model...

Im Focus: Robots as 'pump attendants': TU Graz develops robot-controlled rapid charging system for e-vehicles

Researchers from TU Graz and their industry partners have unveiled a world first: the prototype of a robot-controlled, high-speed combined charging system (CCS) for electric vehicles that enables series charging of cars in various parking positions.

Global demand for electric vehicles is forecast to rise sharply: by 2025, the number of new vehicle registrations is expected to reach 25 million per year....

Im Focus: The “TRiC” to folding actin

Proteins must be folded correctly to fulfill their molecular functions in cells. Molecular assistants called chaperones help proteins exploit their inbuilt folding potential and reach the correct three-dimensional structure. Researchers at the Max Planck Institute of Biochemistry (MPIB) have demonstrated that actin, the most abundant protein in higher developed cells, does not have the inbuilt potential to fold and instead requires special assistance to fold into its active state. The chaperone TRiC uses a previously undescribed mechanism to perform actin folding. The study was recently published in the journal Cell.

Actin is the most abundant protein in highly developed cells and has diverse functions in processes like cell stabilization, cell division and muscle...

Im Focus: Lining up surprising behaviors of superconductor with one of the world's strongest magnets

Scientists have discovered that the electrical resistance of a copper-oxide compound depends on the magnetic field in a very unusual way -- a finding that could help direct the search for materials that can perfectly conduct electricity at room temperatur

What happens when really powerful magnets--capable of producing magnetic fields nearly two million times stronger than Earth's--are applied to materials that...

All Focus news of the innovation-report >>>

Anzeige

Anzeige

VideoLinks
Industry & Economy
Event News

Within reach of the Universe

08.08.2018 | Event News

A journey through the history of microscopy – new exhibition opens at the MDC

27.07.2018 | Event News

2018 Work Research Conference

25.07.2018 | Event News

 
Latest News

Staying in Shape

16.08.2018 | Life Sciences

Diving robots find Antarctic seas exhale surprising amounts of carbon dioxide in winter

16.08.2018 | Earth Sciences

Protein droplets keep neurons at the ready and immune system in balance

16.08.2018 | Life Sciences

VideoLinks
Science & Research
Overview of more VideoLinks >>>