Gain or Loss of Function—Time to Shake up Assumptions on γ-Secretase in Alzheimer Disease?
Aβ40 levels whereas only some drove up Aβ42. Kumar-Singh et al. also found that loss of Ab40 correlated
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Presenilin Loss of Function—Plan B for AD?
dying in droves in an environment of gliosis (Saura et al., 2004). These mice have no amyloid, but they
Messing with the Membrane—An Alternative Interpretation of the Amyloid-β Hypothesis
genetic burden has as yet been described (Oddo et al., 2003). The triple transgenic mouse strain confirmed
Leon Thal Symposium Webinar
On Monday, 27 October 2008, a live Webinar was held by Alzheimer’s research leaders on a national action plan to accelerate discoveries of treatments to prevent dementia. The plan will be presented to the 111th U.S. Congress in March 2009. Presentations w
Betwixt and Intermixed—Dementia With Lewy Bodies
On 15 June 2009, we hosted a Webinar discussion with slide presentations by Ian McKeith at Newcastle University, UK, James Leverenz at University of Washington, Seattle, James Galvin, Washington University, St. Louis, Brit Mollenhauer of Paracelsus-Elena
Herpes Simplex and Alzheimer’s—Time to Think Again?
in the brains of wild-type mice infected with Chlamydia pneumoniae (Little et al., 2004). More
Cell Death: Time to Push It Out of the Doldrums
(Aloyz et al., 1998; Ashkenazi et al., 1998). Death domain sequences vary slightly between receptors, but
Reimagining Alzheimer's Disease—Time for Bright New Ideas?
Alois Alzheimer made a major breakthrough when he discovered senile plaques in the brains of dementia patients, and his work ultimately led to the discovery of amyloid-β and to the amyloid cascade hypothesis. But that cascade is only part of a much bigger
Calcium Signaling Deficit in the Origin of Alzheimer's Disease
1998 May 11;3:a27-31. Abstract. 3. Chen M. The Alzheimer's plaques, tangles and memory deficits
Seeded Aggregation and Transmissible Proteopathy—Creepy Stuff Not Just for Prions Anymore?
can also cause disease characteristics or phenotypes (Collinge et al., 2007). But are prions truly
β Amyloid Degradation: The Forgotten Half of Alzheimer's Disease
activity was attributable to a 110 kDa protease that was later shown to be IDE (Qiu et al., 1998
The Cell Cycle and Alzheimer’s Disease—Let's Unite for Division!
Lin et al., 2001. We have shown that exposure to toxic injuries, such as free radicals, leads to
The AD8—Dementia Screen Ready for Prime Time?
questionnaire to probe cognitive function, and was whittled down to a final eight items (Galvin et al., 2005).
Calcium in AD Pathogenesis
for "amyloid attack" (based on Harvey Pollard’s and Arispe's work; see Lee et al.,
In Search of γ-Secretase
experiment (Wolfe, et al.) are provocative, but they do not conclusively show whether the presenilins are
Have a topic idea for a webinar? We would love to hear it. Send an email to webinars [at] alzforum [dot] org.
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