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a correlation between serum A-β levels and AD (Mehta PD et al., 2001); Vanderstichele H., 2000). Craig Atwood:
allele (Corder et al., 1998)! Objection: If pathogens cause AD, why don't we see AD brains full of
for "amyloid attack" (based on Harvey Pollard’s and Arispe's work; see Lee et al.,
was the Arizona indomethacin study (Rogers et al., 1993). This was not a good study. Other therapeutic
a model of amyotrophic lateral sclerosis (ALS). It is also important to consider that dietary restriction
Neurology (Jack et al., 2010). Jack’s coauthors include clinicians David Knopman and Ron Petersen at Mayo;
tau-positive. Was the reverse true? I ask because if you look at our AD study (Busser et al., 1998), we found
in culture (Skovronsky et al., 1998). Recently, Aβ42 accumulation was reported both in neurons in the
paper by Fassbinder (Fassbinder et al., 2002) on no change in Aβ after statin treatment. Tobias Hartmann
al., 2002; Grön et al., 2005; Chuah and Chee, 2008; FitzGerald et al., 2008). The Alzforum set out to
story and Breitner et al., 2011). Some researchers in the field have not given up hope that reining in
injecting Aβ1-42 more than two years ago (Schenk et al., 1999), I was very surprised they did it in that
See questions answered by Suzanne Hendrix As researchers push into the frontier of early-stage and preventative Alzheimer's disease clinical trials, they will have to measure whether a drug works in people who do not have dementia yet. Traditional ou
June 2012. Preview by Warren et al., 2012 Raj et al., 2012 Zhou et al., 2012 Read a series of questions
neurological disease is the discovery by Hauser et al., recently published in the New England Journal of
Have a topic idea for a webinar? We would love to hear it. Send an email to webinars [at] alzforum [dot] org.
