In work originating from the Bavarian Research Cooperation Prions (FORPRION), which ended in 2007, a team led by the scientist Prof. Dr. Christine Leib-Mösch has been able to show that prion proteins may activate endogenous retroviruses in infected brain cells.
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Researchers have provided new information about how communication among neurons may be prevented from deteriorating in conditions such as Alzheimer’s disease (AD). The new results may lead to new therapies for the treatment of not only AD but also motor neuron diseases and prion diseases.
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Scientists have discovered a new protein that may offer fresh insights into brain function in mad cow disease. “Our team has defined a second prion protein called ‘Shadoo’, that exists in addition to the well-known prion protein called ‘PrP’ ” said Professor David Westaway, director of the Centre for Prions and Protein Folding Diseases at the University of Alberta.
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Studies in mice have indicated that the effects of prion disease could be reversed if caught early enough. The researchers said that their findings support developing early treatments that aim to reduce levels of prion protein in the brains of people with prion disease. Also, they said that their findings suggest testing the efficacy of treatments in a new way: by analyzing their cognitive effects in prion-infected mice.
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