The findings, published in this week's edition of the science journal Nature Genetics, may have implications for therapeutic strategies for some forms of motor neuron disease, Huntington's disease and Alzheimer's.
Late-onset neurodegenerative diseases are a major health burden on the population, yet little is known about the chemical changes that trigger the degeneration of nerve cells. However, many of these diseases are characterised by accumulation, inside nerve cells, of clumps of toxic proteins. The new research - carried out at the Cambridge Institute for Medical Research, the MRC Mammalian Genetics Unit at Harwell and the Department of Genetics, University of Cambridge - has concentrated on tiny molecular motors called dyneins, which are known to be important for moving proteins around inside nerve cells. The researchers found that dyneins play a crucial role in the delivery of toxic proteins to the waste disposal units of cells. When dyneins are defective or absent, this waste disposal system is stalled, clumps of proteins appear, and cell function is compromised.