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-Universitt (LMU) in Munich. At this time it was discovered by accident that mitochondrial toxins can i
|Contact: Dr. Konstanze F. Winklhofer|