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A dead end in neurodegenerative disease research

Munich, 03/06/2012

In science, refuting a hypothesis can be as significant as proving one, all the more so in research aimed at elucidating how diseases proceed with a view toward preventing, treating, or curing them. Such a discovery can save scientists from spending precious years of effort exploring a dead end. In a study published in the Proceedings of the National Academy of Sciences, Munich-based researchers challenge a widely accepted hypothesis about a causative step in neurodegenerative diseases. These results deal specifically with animal models of human amyotrophic lateral sclerosis (ALS, aka Lou Gehrig's disease) but raise questions for research on other neurodegenerative diseases such as Alzheimer's disease and Huntington's disease as well. The lead researchers in this study were Professor Thomas Misgeld of the TUM Institute of Neuroscience, a Fellow of the TUM Institute for Advanced Study, and Professor Martin Kerschensteiner of the LMU Institute of Clinical Neuroimmunology. (PNAS Early Edition, February 27, 2012)

One of the ways neurodegenerative diseases manifest themselves is in the loss of axons – essentially, the transmission lines for electrical signals in individual nerve cells – and synapses, the key sites for communication between them. In the past, such damage has been attributed to deficits in the bidirectional transport of organelles, such as the intracellular power plants called mitochondria, along the axons of nerve cells.

Now, researchers at the Technische Universität München (TUM) and Ludwig-Maximilians-Universität München (LMU) have put that assumption under the microscope in the most thorough test to date. They used novel imaging techniques to observe changes in both axon morphology and organelle transport – with high resolution in both space and time – in several different animal models of ALS. Their results show that transport deficits and axon degeneration can develop independently, refuting the hypothesis that one is a direct cause of the other.

Among the conclusions:  In ALS models, reduction of organelle transport and initiation of axon degeneration appear to be due to different mechanisms. This suggests that, at least for ALS, axonal organelle transport may be an unsuitable therapeutic target. In addition, Misgeld said, "We do think these insights have implications for other studies of ALS, or even studies of other neurodegenerative diseases. In more general biological terms, our results speak to the relationship between axonal transport disruptions and degeneration – which might not be as tight as we assumed. Here we have a lot more to understand." (TU/suwe)

Publikation:
Axonal transport deficits and degeneration can evolve independently in mouse models of amyotrophic lateral sclerosis
Petar Marinkovic, Miriam S. Reuter, Monika S. Brill, Leanne Godinho, Martin Kerschensteiner, and Thomas Misgeld, PNAS Early Edition, Feb. 27-March 2, 2012.
DOI: 10.1073/pnas.1200658109

Contact:
Prof. Martin Kerschensteiner
Institute of Clinical Neuroimmunology
Medical Center of LMU Munich
Phone: +49 89 / 2180 - 78282
E-mail: Martin.Kerschensteiner@med.lmu.de
Web: www.klinikum.uni-muenchen.de/Institut-fuer-Klinische-Neuroimmunologie/en

Prof. Dr. Thomas Misgeld, MD
Institute of Neuroscience
Technische Universität München
Phone.: +49 89 4140 3512
E-Mail:  thomas.misgeld@lrz.tum.de
Web: http://www.misgeld-lab.me.tum.de

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