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 Show me your leaves - Health check for urban trees
12.12.2017 | Gesellschaft für Ökologie e.V.

nachricht Liver Cancer: Lipid Synthesis Promotes Tumor Formation
12.12.2017 | Universität Basel

All articles from Life Sciences >>>

The most recent press releases about innovation >>>

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

Im Focus: Long-lived storage of a photonic qubit for worldwide teleportation

MPQ scientists achieve long storage times for photonic quantum bits which break the lower bound for direct teleportation in a global quantum network.

Concerning the development of quantum memories for the realization of global quantum networks, scientists of the Quantum Dynamics Division led by Professor...

Im Focus: Electromagnetic water cloak eliminates drag and wake

Detailed calculations show water cloaks are feasible with today's technology

Researchers have developed a water cloaking concept based on electromagnetic forces that could eliminate an object's wake, greatly reducing its drag while...

Im Focus: Scientists channel graphene to understand filtration and ion transport into cells

Tiny pores at a cell's entryway act as miniature bouncers, letting in some electrically charged atoms--ions--but blocking others. Operating as exquisitely sensitive filters, these "ion channels" play a critical role in biological functions such as muscle contraction and the firing of brain cells.

To rapidly transport the right ions through the cell membrane, the tiny channels rely on a complex interplay between the ions and surrounding molecules,...

Im Focus: Towards data storage at the single molecule level

The miniaturization of the current technology of storage media is hindered by fundamental limits of quantum mechanics. A new approach consists in using so-called spin-crossover molecules as the smallest possible storage unit. Similar to normal hard drives, these special molecules can save information via their magnetic state. A research team from Kiel University has now managed to successfully place a new class of spin-crossover molecules onto a surface and to improve the molecule’s storage capacity. The storage density of conventional hard drives could therefore theoretically be increased by more than one hundred fold. The study has been published in the scientific journal Nano Letters.

Over the past few years, the building blocks of storage media have gotten ever smaller. But further miniaturization of the current technology is hindered by...

Im Focus: Successful Mechanical Testing of Nanowires

With innovative experiments, researchers at the Helmholtz-Zentrums Geesthacht and the Technical University Hamburg unravel why tiny metallic structures are extremely strong

Light-weight and simultaneously strong – porous metallic nanomaterials promise interesting applications as, for instance, for future aeroplanes with enhanced...

All Focus news of the innovation-report >>>

Anzeige

Anzeige

Event News

See, understand and experience the work of the future

11.12.2017 | Event News

Innovative strategies to tackle parasitic worms

08.12.2017 | Event News

AKL’18: The opportunities and challenges of digitalization in the laser industry

07.12.2017 | Event News

 
Latest News

Long-lived storage of a photonic qubit for worldwide teleportation

12.12.2017 | Physics and Astronomy

Multi-year submarine-canyon study challenges textbook theories about turbidity currents

12.12.2017 | Earth Sciences

Electromagnetic water cloak eliminates drag and wake

12.12.2017 | Power and Electrical Engineering

VideoLinks
B2B-VideoLinks
More VideoLinks >>>