DZNE Scientist Gets Most Important Research Award in Germany

Photo source: DZNE/Laubertphoto

Leibniz Prize goes to Frank Bradke

Bonn, Germany, December 10th, 2015 – The molecular biologist Frank Bradke (46), group leader at the German Center for Neurodegenerative Diseases (DZNE) and professor for neurobiology at the University of Bonn, will be awarded the “Gottfried Wilhelm Leibniz Prize”, which is endowed with 2.5 million euros. The Deutsche Forschungsgemeinschaft (DFG) thereby honors his research on the growth and regeneration of neurons. Through his research Bradke aims to lay the basis for novel therapies, especially for the treatment of spinal cord injuries. „I am overwhelmed und really excited. This is a tremendous recognition for my work“, says the molecular biologist. The award ceremony will be held in Berlin on March 1, 2016.

“We are very proud that Frank Bradke has received this prestigious award”, says Prof. Pierluigi Nicotera, Scientific Director and Chairman of the Executive Board of the DZNE. “Frank Bradke, who is an internationally top-ranked scientist, has very well deserved this prize. His research is based on a full translational approach, therefore opening up new prospects for therapies of neurodegenerative diseases. His personality and his impact on research are extremely important for the DZNE.”

Damaged nerve cells
Nerve cells are wire-like conductors that transmit and receive signals in the form of electrical impulses. This function can be impaired by accidents or disease. Whether or not the affected nerves can recover largely depends on their location: for instance nerve cells in the limbs, the torso and the nose can regenerate to some degree and regain some or all of their function.

In contrast, the neurons in the brain and spinal cord do not have this ability. If they are damaged by accident or disease, the patient is likely to suffer long-term paralysis or other disabilities. But why is regeneration of these neurons and their long nerve fibers, the axons, impeded? This question is the focus of Bradke’s research.

Looking for potential therapies
“Chemicals that block the growth are released by the scar tissue that is formed due to injuries”, says the molecular biologist. “The ideal treatment for promoting axon regeneration after spinal cord injury would inhibit the formation of scar tissue and activate the axons’ regenerative potential”.

In laboratory studies Bradke and his team were able to show that certain cancer drugs can promote the regeneration of nerve cells, while reducing scarring. A corresponding treatment of rats with spinal cord injury significantly improved the animals’ mobility.

“It is certainly still a long way before we may start treating patients. However, we understand better and better what impedes the regeneration of nerve cells. This opens up the possibility of a targeted search for drugs that could perhaps one day be used in clinical practice”, says Bradke. “The Leibniz Prize is a confirmation that we are on the right track. This award will open up entirely new ways for our team to continue our research.”

The awardee
After studying at the Freie Universität Berlin and University College London, Bradke initially carried out research at the European Molecular Biology Laboratory (EMBL) in Heidelberg as part of his doctoral thesis. As a postdoctoral researcher, he moved to the University of California in San Francisco and Stanford University in 2000. In 2003, he was appointed a group leader at the Max Planck Institute of Neurobiology in Martinsried. In 2011, he was awarded the IRP Schellenberg Prize, one of the highest awards in the field of regeneration research. In the same year, he became full professor at the University of Bonn, and was appointed head of the Axon Growth and Regeneration working group at the DZNE.

In 2013, Frank Bradke was elected a member of the European Molecular Biology Organization (EMBO), members of which are the world’s most renowned molecular biologists. In 2014 he was elected into the Leopoldina, the German National Academy of Sciences.

Dr. Dirk Förger
Press Spokesman, DZNE
+49 (0) 228 / 43302-260

More information: German Research Foundation (DFG)

New research sheds light on neuronal communication

Researchers at the Max Planck Florida Institute for Neuroscience have uncovered a critical molecule that regulates synaptic transmission

– Neurons communicate with each other through specialized structures called synapses.
– The information is transmitted in the form of synaptic vesicles that contain specific chemical messengers called neurotransmitters
– The amount and coordinated release of neurotransmitters regulates synaptic strength which is critical to maintain proper communication between neurons.
– To better understand and address a number of neurological disorders, we need a better understanding of the molecular mechanisms that regulate neuronal communication.
– A new study has revealed an important function of a class of presynaptic proteins previously implicated in neurological disorders in the regulation of synaptic strength.

Synaptic proteins and neuronal transmission

A synapse consists of a presynaptic terminal of one neuron and a postsynaptic terminal of another. The presynaptic terminal stores vesicles containing neurotransmitters, while the postsynaptic terminal contains neurotransmitter receptors. A dense collection of proteins is present in these terminals, however the functional role of many of these proteins remains unknown.

In particular, the G-protein-coupled receptor kinase-interacting proteins (GITs) exert a critical control in synaptic transmission, since deletions of these proteins are lethal or cause sensory deficits and cognitive impairments in mice. In particular, GIT proteins and the pathways they regulate have been implicated in neurological disorders such as Attention Deficit Hyperactivity Disorder (ADHD) and Huntington’s Disease. Several studies have demonstrated the role of GITs in the postsynaptic terminal, but very little is known about their role in the presynaptic terminal. Researchers in Samuel Young Jr.’s research team at the Max Planck Florida Institute for Neuroscience set out to investigate the role of GITs in the giant synapse, the calyx of Held, of the auditory system – the optimal model to study the presynaptic terminal independently from the postsynaptic terminal.

New findings

In their December publication in Neuron, Drs. Samuel Young Jr. and Mónica S. Montesinos and collaborators report for the first time that GIT proteins are critical presynaptic regulators of synaptic strength. This study uncovers previously unknown distinct roles for GIT1 and GIT2 in regulating neurotransmitter release strength, with GIT1 as a specific regulator of presynaptic release probability. This regulation is likely to contribute to the disruptions in neural circuit functions leading to sensory disorders, memory and learning impairment and other neurological disorders

Future Directions

Future studies of Dr. Samuel Young Jr.’s lab will resolve the mechanisms by which GITs regulate synaptic strength and their roles in the early stages of auditory processing and neurological diseases. “Our work brings significant insight into the understanding of how neuronal communication is regulated, which is essential to understand the cellular and molecular mechanisms of information processing by neuronal circuits and the role of these proteins in the development of neurological diseases,” explained Dr. Young.


Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse

Mónica S. Montesinos, Wei Dong, Kevin Goff, Brati Das, Debbie Guerrero-Given, Robert Schmalzigaug, Richard T. Premont, Rachel Satterfield, Naomi Kamasawa, Samuel M. Young Jr.

Neuron, Volume 88, Issue 5, 02 December 2015, Pages 918–925.