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Dr. Derek Bowie has recently been appointed to the Editorial Board of the
Journal of Physiology and was reported in the Spring Edition of the Physiology News
Anne-Marie Downey, an MSc student in Bernard Robaire’s lab, was awarded a Research Excellence Trainee Award / Anna Steinberger Award from the American Society of Andrology for 2012-2014
for her abstract entitled: "Cyclophosphamide Treatment Affects miRNA Expression Profiles in Male Rat Germ Cells"
Geraldine Longo, a PhD student in Alfredo Ribeiro-da-Silva’s lab, has received a Louise and Alan Edwards Foundation’s Edwards PhD. Studentship in Pain Research for 2012.
Michael Accardi, a PhD student in Derek Bowie’s lab, has received the Gelder-Savoy studentship award for 2012-2013 from the Savoy Foundation.
Geraldine Longo, a PhD student in Alfredo Ribeiro-da-Silva's lab, has received an award from the International Association for the Study of Pain (IASP) to attend the World Congress on pain in Milan, summer of 2012.
Raminder Gill, a PhD student in Anne McKinney’s lab, has won a student fellowship from the Savoy Foundation on Epilepsy.
David Verbich, a PhD student in Anne McKinney’s lab, has won the CIHR Canadian Graduate Scholarship - Michael Smith Foreign Study Supplement.
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Daniela Kaden, Anja Harmeier, Christoph Weise, Lisa M. Munter, Veit Althoff, Benjamin R. Rost, Peter W. Hildebrand, Dietmar Schmitz, Michael Schaefer, Rudi Lurz,
Sabine Skodda, Raina Yamamoto, Sönke Arlt, Ulrich Finckh, Gerd Multhaup
Novel APP/Aß mutation K16N produces
highly toxic heteromeric Aß oligomers
EMBO Mol Med. 2012 Apr 19. doi: 10.1002/emmm.201200239. [Epub ahead of print]
The paper characterizes a novel mutation in the amyloid precursor protein (APP) resulting in early onset dementia of the Alzheimer type with an autosomal dominant inheritance pattern. The missense mutation is located directly at the a-secretase cleavage site (APP K16N, according to amyloid-ß (Aß) numbering) and influences both APP processing and Aß level. First, due to the K16N mutation APP secretion is affected and higher amounts of Aß peptides are being produced. Second, unexpectedly Aß peptides carrying the K16N mutation are not harmful to neuronal cells but gain considerable toxicity when mixed with its wild type counterpart, mimicking the heterozygous state of the subject. Furthermore, Aß42 K16N peptides inhibit fibril formation of Aß42 wild-type. Even more, Aß42 K16N peptides are protected against clearance activity by one of the major Aß-degrading enzymes neprilysin. Thus the mutation described here harbors a combination of risk factors that may synergistically contribute to the development of early onset Alzheimer disease.
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