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Z-Phe-Ala-diazomethylketone (PADK) disrupts and remodels early oligomer states of the Alzheimer disease Aβ42 protein.
Zheng X, Gessel MM, Wisniewski ML, Viswanathan K, Wright DL, Bahr BA, Bowers MT.
J Biol Chem. 2012 Feb 24;287(9):6084-8. Epub 2012 Jan 17.
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Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia.
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SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid β protein oligomerization and memory loss in mouse model of Alzheimer disease.
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Exosome-associated tau is secreted in tauopathy models and is selectively phosphorylated in cerebrospinal fluid in early Alzheimer disease.
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Polar transmembrane-based amino acids in presenilin 1 are involved in endoplasmic reticulum localization, Pen2 protein binding, and γ-secretase complex stabilization.
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Amyloid-β-induced synapse damage is mediated via cross-linkage of cellular prion proteins.
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Taking a load off the brain.
[No authors listed]
J Biol Chem. 2011 Oct 28;286(43):e99971. No abstract available.
BRI2 protein regulates β-amyloid degradation by increasing levels of secreted insulin-degrading enzyme (IDE).
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Ubiquilin-1 is a molecular chaperone for the amyloid precursor protein.
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Testing the therapeutic potential of doxycycline in a Drosophila melanogaster model of Alzheimer disease.
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Receptor for advanced glycation end products (RAGE) prevents endothelial cell membrane resealing and regulates F-actin remodeling in a beta-catenin-dependent manner.
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Passive immunization with anti-Tau antibodies in two transgenic models: reduction of Tau pathology and delay of disease progression.
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Interactions of pathological hallmark proteins: tubulin polymerization promoting protein/p25, beta-amyloid, and alpha-synuclein.
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J Biol Chem. 2011 Sep 30;286(39):34088-100. Epub 2011 Aug 8.
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