Are Neurons Just Too Laissez-Faire about Repair?
do not efficiently repair the bulk of their genome (see, for example, Gobbel et al., 1998). Neurons
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do not efficiently repair the bulk of their genome (see, for example, Gobbel et al., 1998). Neurons
hypothesis of Ab and related Ab-lowering strategies in more breadth and detail. Synposis of Deane et al
(Cai et al., 2002; Naruse et al., 1998; ARF related news story). One way in which PS1 might modulate
caused the sprouting. See our paper in J Neuroscience in November (Sheng et al., 2002). Milos Ikonomovic
oligomerize and polymerize out of lipid environment, to self- and cross-associate (Koudinov et al., 1998
1992; Cogoni et al., 1996). Since its first description in animal cells (Fire et al., 1998), a growing
al., 2000; Weller et al., 1998). Moreover, in transgenic mice, virtually identical amyloid-associated
Jiang et al., 1998), together with the commercial availability of PPARγ agonists, has raised interest in
out there! (See Jaworska-Wilczynska et al., 2002.) Jorge Busciglio Gunnar, you see particularly
paper by Fassbinder (Fassbinder et al., 2002) on no change in Aβ after statin treatment. Tobias Hartmann
One paper showed Ab to bind to APP. Does this seem reasonable? (See Lorenzo, et al., Nature Neurosci
activity was attributable to a 110 kDa protease that was later shown to be IDE (Qiu et al., 1998
Lin et al., 2001. We have shown that exposure to toxic injuries, such as free radicals, leads to
Ashford, Soultanian, et al., 1999. We did not examine axons. However, this discussion seems to be focusing
Mice lacking both PS1 and PS2 die before embryonic day 9 (Donoviel et al., 1999). PS1-/- mice, which
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