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In 2002, a group of scientists at the University of Toronto was able to identify a gene which they dubbed DREAM (downstream regulatory element antagonistic modulator). The gene's function was highly interesting: it obviously served as a key regulator in the perception of pain. Mice who lacked the gene showed clear signs of markedly reduced sensitivity to all kinds of pain, whether chronic or acute. Otherwise, the mice appeared perfectly normal.
The work leading to these findings was carried out in the lab of Josef Penninger, then principal investigator at the Amgen Institute in Toronto. The publication describing the gene's function was received with great interest (Cell, Vol. 108, 31-43, 11.1.2002) and DREAM was subsequently termed the "Master-Gene of pain perception".
Josef Penninger, meanwhile scientific director of IMBA, the Institute of Molecular Biotechnology of the Austrian Academy of Sciences in Vienna, continued to wonder what other surprises DREAM might have in store. In a collaborative effort with neurobiologists from the University Pablo de Olivade (Seville) he devised experiments to follow up on the previous findings. A team of scientists under ngel Manuel Carrin subjected DREAM-less mice to numerous neurological tests and analyzed their memory skills. The results were striking: without DREAM, mice were able to learn faster and remember better. Fascinatingly, the brains of aged mice (18 months) showed learning capacities similar to those of very young mice.
Thus, DREAM turns out to be a genetic candidate for explaining old age dementia. Even a causal connection to Alzheimer's disease seems plausible. Studies published in mid 2008 suggest that the devastating condition may be related to Calcium regulation gone awry. The accumulation of amyloid plaques in brain cells, usually
|Contact: Dr. Heidemarie Hurtl|
Research Institute of Molecular Pathology