The Pathogen Hypothesis—Challenging the Primacy of Genetics in Late-Onset Alzheimer Disease.
allele (Corder et al., 1998)! Objection: If pathogens cause AD, why don't we see AD brains full of
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allele (Corder et al., 1998)! Objection: If pathogens cause AD, why don't we see AD brains full of
deposition in APP mice, a result observed in three separate laboratories (see Patel et al., 2005 and Wang et
injury (see Bush et al., 1999). Gabrielle Strobel And I believe Tony Wyss-Coray has data on active
(see Constantini et al., 2005) where we show that ceramide levels increase during aging in the brain of
(Lopez et al., 2005). Eli Michaelis Thanks, June. Jens Eckstein The problem is that adoption of
aged 78 postmortem, did not have APP pathology (see Prasher et al., 1998). She was trisomic for the
are very interesting! Natalie Rasgon Currently, there are studies (see, for example, Benedict et al.,
regarding your peptide inhibitor (see Sadowski et al., 2004)? In your paper, your peptide inhibits the
disease, the mutated protein also disturbs function of skin cells in patients (according to Seo et al.,
et al., 1998; Lin et al., 1999; Lin et al., 2001; Bhatia et al., 2000). Tom Fagan So how does the
milestone paper by Pratico et al., 2001 on isoprostanes in AD and also papers by Montine et al., 2005 and
samples). (See Kung et al., 2002.) The data look good but we are not ready to publish yet. Bill, what's
a model of amyotrophic lateral sclerosis (ALS). It is also important to consider that dietary restriction
Einstein College of Medicine in 1997 (see Heitner et al., 1997) and found nothing, but it was spotty
protection against the Aβ toxicity (see Lovell et al., 1998). All told, the evidence points to iron- or
Have a topic idea for a webinar? We would love to hear it. Send an email to webinars [at] alzforum [dot] org.