Borrowed from the yahoo board - any comments from the experts here?
Amyloidosis impairs cognitive function
by: pfaffova (33/M/Heidelberg) 01/09/05 10:32 am
Msg: 513700 of 513721
The holy grail!
Hold on to your shares until we get a look at the one year PII Alzheimer data. If those brain scans by General Electric allow us to correlate decreasing plaque levels with increased cognitive function, then the world of old-folks is truely going to be a better place. Lets hope the side effect profile is similar/better to that of Tysabri.
nature.com. html&dynoptions=doi1105284413
Article
Nature Neuroscience 8, 79 - 84 (2004)
Published online: 19 December 2004; | doi:10.1038/nn1372
Natural oligomers of the amyloid- protein specifically disrupt cognitive function
James P Cleary1, 2, Dominic M Walsh3, 4, Jacki J Hofmeister1, Ganesh M Shankar3, Michael A Kuskowski1, 5, Dennis J Selkoe3 & Karen H Ashe1, 6
1 Geriatric Research, Education and Clinical Center, Minneapolis Veterans Affairs Medical Center, Minneapolis, Minnesota 55417, USA.
2 Department of Psychology, University of Minnesota, Minneapolis, Minnesota 55455, USA.
3 Department of Neurology, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
4 Laboratory for Neurodegenerative Research, Conway Institute of Biomedical and Biomolecular Research, University College Dublin, Belfield, Dublin 4, Republic of Ireland.
5 Department of Psychiatry, University of Minnesota, Minneapolis, Minnesota 55455, USA.
6 Department of Neurology, 420 Delaware Street SE, MMC #295, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Correspondence should be addressed to Karen H Ashe hsiao005@umn.edu
A central unresolved problem in research on Alzheimer disease is the nature of the molecular entity causing dementia. Here we provide the first direct experimental evidence that a defined molecular species of the amyloid- protein interferes with cognitive function. Soluble oligomeric forms of amyloid-, including trimers and dimers, were both necessary and sufficient to disrupt learned behavior in a manner that was rapid, potent and transient; they produced impaired cognitive function without inducing permanent neurological deficits. Although -amyloidosis has long been hypothesized to affect cognition, the abnormally folded protein species associated with this or any other neurodegenerative disease has not previously been isolated, defined biochemically and then specifically characterized with regard to its effects on cognitive function. The biochemical isolation of discrete amyloid- moieties with pathophysiological properties sets the stage for a new approach to studying the molecular mechanisms of cognitive impairment in Alzheimer disease and related neurodegenerative disorders.
Disclaimer: This article was first posted by viergeinvest.
PS Does anybody have the full-text version???
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