Could a New Down Syndrome Mouse Model Also Be Useful for Alzheimer Research?
aged 78 postmortem, did not have APP pathology (see Prasher et al., 1998). She was trisomic for the
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aged 78 postmortem, did not have APP pathology (see Prasher et al., 1998). She was trisomic for the
Dean? William Klein: Let me start by saying how much I enjoyed the paper by Dean et al. A good read.
regarding your peptide inhibitor (see Sadowski et al., 2004)? In your paper, your peptide inhibits the
reflect Alzheimer’s disease in the brain (see review by Toledo et al., 2013). Attempts to correlate other
hypothesis of Ab and related Ab-lowering strategies in more breadth and detail. Synposis of Deane et al
decreases in proteasome activity in AD (Keller et al., 2000 and Keck et al., 2003, but has anyone looked
concept of synaptic apoptosis developed by Mattson et al., 1998 John Q. Trojanowski One would assume
disease, the mutated protein also disturbs function of skin cells in patients (according to Seo et al.,
important roles of protein acetylation. I am also referring to this month’s paper by Creppe et al., 2009 on
are very interesting! Natalie Rasgon Currently, there are studies (see, for example, Benedict et al.,
this approach to identify molecular modules that might contribute to metabolic syndrome (Chen et al.,
was the Arizona indomethacin study (Rogers et al., 1993). This was not a good study. Other therapeutic
out there! (See Jaworska-Wilczynska et al., 2002.) Jorge Busciglio Gunnar, you see particularly
samples). (See Kung et al., 2002.) The data look good but we are not ready to publish yet. Bill, what's
Fe65 knockout (KO) mice (see Guenette et al., 2006) and Ulrike Muller showed with her APP triple KO
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