11625 RESULTS
COMMENT The identification of genes for Mendelian forms of Parkinson disease (PD) has greatly advanced the understanding of the molecular pathogenesis of this common neurodegenerative disorder. The discovery of mutations in the gene for α-synuclein (SNCA; PARK1)
COMMENT This theory seems to fit neatly, without being sliced up by Occam's Razor. Do I now try to drink more tap water? 0 pietvana
COMMENT I concur with the other comments: The in-vivo M1 agonist treatment effect on Aß is very
COMMENT This is an interesting paper that describes a clever approach for targeting amyloid-β and preventing further aggregation. It is particularly interesting that a relatively uniform Aβ oligomer results from treatment that prevents the formation of fibrils. T
COMMENT The ability of the M1 agonist AF267B to decrease amyloid plaque load, decrease tau phosphorylation, and enhance memory function in the "triple transgenic" mice is indeed encouraging. Selective muscarinic agonists are among the few therapeutic ap
COMMENT In the 29 October issue of Science, Gestwicki, Crabtree, and Graef report results of a beautiful series of experiments testing the hypothesis that small-molecule inhibition of protein assembly can work, as long as the inhibitor isn't small! Gestwicki
COMMENT I think this is among the most important observations shown at the meeting. I had seen Frank LaFerla’s behavior data and antibody reversal earlier in September at a meeting on cognition. It supports and is consistent with the results from most of the mice
COMMENT The triple transgenic animals are a fascinating addition to the tools available. Especially exciting is this new data indicating that these genes have to work together in order to convert mice to an AD model. Obviously, these mice remain an animal model o
COMMENT This data confirms our work, done in collaboration with Abraham Fisher, showing that AF267B and two other of his M1 agonists (AF102B, AF150S) all lower CSF and cortical Aβ concentrations in normal rabbits [1]. This confirms many years of in vitro work goi
COMMENT If this data holds true, it is very good news in the field. Abe Fisher has been working for years to develop highly specific muscarinic (M1) agonists. He is more advanced on that than anyone else, as the major pharmaceutical companies have abandoned that
COMMENT There has been, for obvious reasons, a tremendous research effort investigating the role of tau protein and synuclein protein as the building blocks for filaments in neruofibrillary tangles, Lewy bodies and glial cytoplasmic inclusions. However, it is nic
COMMENT Contrary to the title, this study is limited to the usual suspects: Abeta 40 and 42 and PS1. The study does offer the advantage of segregating cases by early onset/late onset and presence of PS1 mutations, though the abstract does not clarify how the PS1
COMMENT Posttranslational processing of proteins clearly serves vital functions in normal and diseased cellular functioning. It is refreshing to see tau examined with regard to something other than phosphorylation/truncation, though this is not the first paper to
COMMENT mentioned in these comments will lead to expanded efforts in pathogen associations in neurodegenerative
COMMENT The identity of substrates of γ-secretase is becoming more and more interesting—although the wealth of putative candidate substrates is also becoming somewhat disturbing. Scrutinizing all of them to define the exact physiological role (if any) of the proc
