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uni'wissen 01-2012_ENG

Biological networks of nerve cells (left) and a schema of the network (right) that can serve as the basis for computer simulations: Computational neuroscience uses equations and models to determine how the human brain functions. Guiding a cup to one’s mouth is a simple ­process, and yet it involves the joint action of millions of nerve cells. For the 300,000 million people in Germany suffering from Parkinson’s disease, it thus presents a real problem. Particu­ larly in the later stages of the disease, patients can only carry out deliberate movements with great effort, if at all. The disease originates in the basal ganglia, a group of structures in the brain that are among other things responsible for selecting and ­controlling movements. In Parkinson’s patients, nerve cells in these structures that produce and store the chemical messenger dopamine die off for reasons that are as yet unclear. The shortage of dopamine disrupts the balance between inhib­ iting and stimulating substances in the process­ ing and transmitting of impulses. By the time the first disturbances in motion sequences appear, more than half of the cells producing dopamine have already died off. “Since the outward signs aren’t visible until so late, we don’t know exactly where the disease originates,” says Dr. Arvind Kumar from the Bernstein Center Freiburg and “When something is so microscopically small that I don’t see it and at the same time so complex that I don’t understand it, I have to simplify it” the Faculty of Biology of the University of Freiburg. The engineer and theoretical neurosci­ entist is thus working with hypotheses: A computer model he has developed proposes an explana­ tion of how Parkinson’s disease emerges – and of how deep brain stimulation (DBS) counteracts the symptoms. A Parkinson’s therapy begins with drugs that compensate for the lack of dopamine. But in the course of time the drug’s duration of effect ­decreases and phases of good movement can end abruptly – the so-called on-off phenomenon. The use of DBS, a neurosurgical procedure that can alleviate the symptoms, was approved in 1998. The patient receives a so-called neuro­ stimulator as an implant: Electrodes are placed at certain positions in the brain through a tiny hole in the cranium. An impulse generator con­ nected to the electrodes sends weak electrical impulses, causing a permanent electrical stimu­ lation to act on abnormally overactive nerve cells. The procedure does not destroy any brain tissue, and the intensity and voltage of the current can be adjusted at any time with a programming 17