By Douglas R. O. Morrison (auth.), Prof. Douglas R. O. Morrison (eds.)
Most of the world's specialists on prions met for a workshop in Erice in August 1996. the purpose of the workshop was once to debate the basics of the technological know-how ofprions. It was once for tunate that such a lot of might be current given the strain that they have been lower than as a result of the information provided in March 1996, indicating that Bovine Spongiform Encephalopathy, BSE or Mad Cow illness, had penetrated the species barrier and was once commencing to reason a brand new dis ease in humans--the new version ofCreutzfeldt-Jakob disorder, nvCJD. this significant and pressing topic turned an extra significant subject on the workshop. it is a publication containing many of the talks plus the abstracts of these not able to discover time to jot down up their talks. just about all papers have been written within the spring and summer season of 1997 and comprise fabric extra after the workshop; hence Bob Will's paper at the new version of cm comprises info as much as July 1997 and 4 contributions arrived in October 1997. as well as the talks given at our workshop, there has been a unique joint consultation with the Planetary Emergencies Workshop the place many distinctive scientists, together with 3 Nobel laureates, mentioned significant concerns affecting our planet. Six talks got through us to this different workshop, 5 approximately prions, BSE, and nvCJD, and one at the broader factor of recent epi demics by way of Luc Montagnier. even if many of the talks involved study matters, there have been a number of specified talks.
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Example text
16 15. COMPARISON OF PRION DISEASES WITH ALZHEIMER'S DISEASE David Westaway gave a second talk on Alzheimer's Disease, AD. He first described it, gave a thought-provoking comparison with some prion diseases, and reported on experiments using transgenic mice which had presenilin 1, PSI. So far factors causing AD are a) missense mutations in the presenilin 1, PSI, gene on chromosome 14, b) missense mutations in the presenilin 2, PS2, gene on chromosome 1, and c) rare mutations on the APP gene on chromosome 21.
5:13-21 (1995). M. Sallanon, C. Aubert, M. Denoyer, K. Kitaharna, M. 10uvet, L'insomnie consecutive II la lesion de la region preoptique paramediane est reversible par inactivation de l'hypothalamus posterieur chez Ie chat, CR Acad Sci [III] 305:561-567 (1987). C. A. P. Goldberg, Pseudo hypersomnia and pre-sleep behaviour with bilateral paramedian thalamic lesions, Brain 116: 1549-1563 (1993). C. Bassetti, 1. Mathis, M. O. W. Hess, Hypersomnia following paramedian thalamic stroke: a report of 12 patients.
Spongiform change, often considered a characteristic of prion diseases, may be absent or mild in certain mutations of GSS. It may also be an important clue that PSI, PS2, APP and PrP are all associated with the cell membrane. Maurizio Pocchiari compared amyloidosis in prion diseases, Alzheimer's Disease, and Transthyretin, TIR. A table is given with various disease types of TIR, corresponding mutations (where known) and the composition of the amyloid protein. Similarities are noted and the possibility is explored that all three are "conformational disease" where folding plays a critical role.