Deficiency of Presenilin 1 Inhibits the Normal Cleavage of the Transmembrane Domain of Amyloid Precursor Protein
report by De Strooper et. al., (1),and the accompanying commentary by Haas and Selkoe (2), conclude that
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Hemochromatosis as a Factor in AD
evidence (Connor et al.) that the HFE protein is found on brain capillaries, choroid plexus and ependymal
Cholesterol and Alzheimer's—Charging Fast But Still at a Distance from Solid Answers
paper by Fassbinder (Fassbinder et al., 2002) on no change in Aβ after statin treatment. Tobias Hartmann
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
Axonal Transport Hypothesis Moves On to Implicate Presenilin
(Cai et al., 2002; Naruse et al., 1998; ARF related news story). One way in which PS1 might modulate
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
Cast Call for Players: Healthy Aging Through Lean Living
was no different than that of the animals fed ad libitum every day (see Anson et al., 2003). Howard
Latest γ-Secretase Substrate Involved in Synaptic Stability, Autism?
Südhof, 2008, review; Yanagi et al., 2012; Sun et al., 2011; Qi et al., 2009). Two papers in the October
Alzheimer Genes in Cortical Development: How Do Their Prenatal Functions Relate to Dementia?
Mice lacking both PS1 and PS2 die before embryonic day 9 (Donoviel et al., 1999). PS1-/- mice, which
Frameshift Mutants of β Amyloid Precursor Protein and Ubiquitin-B in Alzheimer's and Down's Syndrome Patients
aberrant splicing events exclusively in sporadic ALS patients (Lin et al., 1998). The splice variants were
How the Other Half Lives—Or the What, How, and Where of the AβPP Intracellular Domain
One paper showed Ab to bind to APP. Does this seem reasonable? (See Lorenzo, et al., Nature Neurosci
The Pathogen Hypothesis
associated mental impairment in mice (see Aleksandrova et al., 2004). Thus the need for many more controls to
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
Calcium in AD Pathogenesis
for "amyloid attack" (based on Harvey Pollard’s and Arispe's work; see Lee et al.,
Together at Last, Top Five Biomarkers Model Stages of AD
Neurology (Jack et al., 2010). Jack’s coauthors include clinicians David Knopman and Ron Petersen at Mayo;
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