An international team of researchers identified a pathogenic mechanism that is common to several neurodegenerative diseases. The findings suggest that it may be possible to slow the progression of dementia even after the onset of symptoms.
The relentless increase in the incidence of dementia in aging societies poses an enormous challenge to health-care systems. An international team of researchers led by Professor Christian Haass and Gernot Kleinberger at the LMU's Adolf-Butenandt-Institute and the German Center for Neurodegenerative Diseases (DZNE), has now elucidated the mode of action of a genetic defect that contributes to the development of several different dementia syndromes.
Neurodegenerative disorders such as Alzheimer's and Parkinson's diseases or frontotemporal dementia display a number of common features. They are all characterized by the appearance in the brains of affected patients of abnormally high levels of insoluble protein deposits, which are associated with massive loss of nerve cells. In order to minimize further damage to nerve cells in the vicinity of such deposits, dead cells and the proteinaceous aggregates released from them must be efficiently degraded and disposed of. This task is performed by specialized phagocytic cells the so-called microglia which act as "sanitary inspectors" in the brain to ensure the prompt removal of debris that presents a danger to the health of nearby cells. Microglia are found only in the central nervous system, but functionally they represent a division of the body's innate immune system.
As Haass and his colleagues now report in the latest issue of the journal Science Translational Medicine, specific mutations in the gene for a protein called TREM2, which regulates the uptake of waste products by microglia, lead to its absence from the cell surface. TREM2 is normally inserted into the plasma membrane of microglial cells such that part of it extends through the membran
|Contact: Luise Dirscherl|