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Neurodegenerative diseases: Glitch in garbage removal enhances risk
Date:7/3/2014

e as an extracellular domain. This exposed portion of TREM2 is responsible for the recognition of waste products left behind by dead cells. "We believe that the genetic defect disrupts the folding of the protein chain soon during its synthesis in the cell, so that it is degraded before it can reach the surface of the microglia," says Kleinberger. As a result, the amount of debris that the microglia can cope with is significantly reduced. Consequently, the toxic protein deposits, as well as whole dead cells, cannot be efficiently removed and continue to accumulate in the brain. This is expected to trigger inflammatory reactions that may promote further nerve-cell loss.

The new study thus pinpoints a mechanism that influences the course of several different brain diseases. "In addition, our findings may perhaps point to ways of slowing the rate of progression of these illnesses even after the manifestation of overt signs of dementia, which has not been possible so far," says Haass. "That this may indeed be feasible is suggested by the initial results of an experiment in which we were able to stimulate the phagocytic activity of microglia by pharmacological means."


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Contact: Luise Dirscherl
presse@lmu.de
0049-892-180-3423
Ludwig-Maximilians-Universitt Mnchen
Source:Eurekalert

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