Gain or Loss of Function—Time to Shake up Assumptions on γ-Secretase in Alzheimer Disease?
Davies of Albert Einstein College of Medicine in the Bronx, New York, and Bart De Strooper at K.U.
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Davies of Albert Einstein College of Medicine in the Bronx, New York, and Bart De Strooper at K.U.
fortuitous timing, Bart de Strooper and Michael Wolfe have written their own analysis of the existing data on
accumulation of the Aβ peptide plays an important role in AD. Yet Marchesi's ideas come at a time when
Prevention of Dementia (LTS’08) and the Alzheimer’s Study Group (ASG) to solicit suggestions from the
mixed disease. In DLB, patients suffer from various combinations of Alzheimer and Parkinson signs, which
work on herpes simplex virus type 1 (HSV1) and Brian Balin ’s data showing induction of amyloid plaques
diseases such as Alzheimer's and Parkinson's (Driscoll and Gerstbrein, 2003; Zhang et al., 2002)
Jersey, believes that the time has come to reassess what we know about AD, focusing less on amyloid and
when Ca2+ signal is reduced, tau will accumulate and at the same time become hyperphosphorylated. 6.
Alzheimer, Parkinson, and Huntington diseases, amyotrophic lateral sclerosis (ALS), and prion diseases, such
today's chat. I am Gabrielle Strobel, managing editor of the Alzheimer Research Forum, and will be
welcoming everyone to this discussion on the cell cycle and Alzheimer's disease. Let’s cycle! The basic
the clinical dementia rating scale and against neuropsychological tests, and is available in several
neurodegeneration in the Alzheimer's mouse brain despite chronic high Ca2+ varicosities and blebs? Brian
some responses on other topics? Perhaps a role for ApoE? The connection of Alzheimer's disease and
Have a topic idea for a webinar? We would love to hear it. Send an email to webinars [at] alzforum [dot] org.