Associated Papers
Cholesterol-lowering drugs reduce APP processing to Aβ by inducing APP dimerization.
Langness VF et al.
Molecular Biology of the Cell, 2021
Cholesterol Metabolism Is a Druggable Axis that Independently Regulates Tau and Amyloid-β in iPSC-Derived Alzheimer's Disease Neurons.
van der Kant R et al.
Cell Stem Cell, 2019
Stem Cell-Derived Neurons as Cellular Models of Sporadic Alzheimer's Disease.
Foveau B et al.
Journal of Alzheimer's Disease : Jad, 2019
Specific Binding of Cholesterol to the Amyloid Precursor Protein: Structure of the Complex and Driving Forces Characterized in Molecular Detail.
Nierzwicki Ł et al.
The Journal of Physical Chemistry Letters, 2015
Modeling Alzheimer's disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness.
Kondo T et al.
Cell Stem Cell, 2013
The E693Delta mutation in amyloid precursor protein increases intracellular accumulation of amyloid beta oligomers and causes endoplasmic reticulum stress-induced apoptosis in cultured cells.
Nishitsuji K et al.
The American Journal of Pathology, 2009
A new amyloid beta variant favoring oligomerization in Alzheimer's-type dementia.
Tomiyama T et al.
Annals of Neurology, 2008
The C99 domain of the amyloid precursor protein resides in the disordered membrane phase.
Capone R et al.
The Journal of Biological Chemistry, 0
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