Knock-in rats with homozygous PSEN1L435F Alzheimer mutation are viable and show selective γ-secretase activity loss causing low Aβ40/42 and high Aβ43

Opposite changes in APP processing and human Aβ levels in rats carrying either a protective or a pathogenic APP mutation

(2020) Marc D Tambini et al.   eLife

A cellular complex of BACE1 and γ-secretase sequentially generates Aβ from its full-length precursor

(2019) Lei Liu et al.   JOURNAL OF CELL BIOLOGY

Secreted amyloid-β precursor protein functions as a GABABR1a ligand to modulate synaptic transmission

(2019) Heather C. Rice et al.   SCIENCE

Tuning of glutamate, but not GABA, release by an intra-synaptic vesicles APP domain whose function can be modulated by β- or α-secretase cleavage

(2019) Wen Yao et al.   JOURNAL OF NEUROSCIENCE

Facilitation of glutamate, but not GABA , release in Familial Alzheimer's APP mutant Knock‐in rats with increased β‐cleavage of APP

(2019) Marc D. Tambini et al.   AGING CELL

The Many Substrates of Presenilin/γ-Secretase

(2018) Annakaisa Haapasalo et al.   JOURNAL OF ALZHEIMERS DISEASE

Intraneuronal aggregation of the β-CTF fragment of APP (C99) induces Aβ-independent lysosomal-autophagic pathology

(2016) Inger Lauritzen et al.   ACTA NEUROPATHOLOGICA

Generation and deposition of Aβ43 by the virtually inactive presenilin‐1 L435F mutant contradicts the presenilin loss‐of‐function hypothesis of Alzheimer's disease

(2016) Benedikt Kretner et al.   EMBO Molecular Medicine

Familial Alzheimer’s Disease Mutations in Presenilin Generate Amyloidogenic Aβ Peptide Seeds

(2016) Sarah Veugelen et al.   NEURON

Analysis of 138 pathogenic mutations in presenilin-1 on the in vitro production of Aβ42 and Aβ40 peptides by γ-secretase

(2016) Linfeng Sun et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Physical and functional interaction between the α- and γ-secretases: A new model of regulated intramembrane proteolysis

(2015) Allen C. Chen et al.   JOURNAL OF CELL BIOLOGY

Presenilin-1 Knockin Mice Reveal Loss-of-Function Mechanism for Familial Alzheimer’s Disease

(2015) Dan Xia et al.   NEURON

APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses

(2015) Tomas Fanutza et al.   eLife

Partial Loss of Presenilin Impairs Age-Dependent Neuronal Survival in the Cerebral Cortex

(2014) H. Watanabe et al.   JOURNAL OF NEUROSCIENCE

Inhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia

(2012) Robert Tamayev et al.   Molecular Neurodegeneration

β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia

(2011) Robert Tamayev et al.   EMBO Molecular Medicine

Functions of Aβ, sAPPα and sAPPβ : similarities and differences

(2011) Stéphanie Chasseigneaux et al.   JOURNAL OF NEUROCHEMISTRY

A Presenilin-1 Mutation Identified in Familial Alzheimer Disease with Cotton Wool Plaques Causes a Nearly Complete Loss of γ-Secretase Activity

(2010) Elizabeth A. Heilig et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Synergistic Tissue Counterstaining and Image Segmentation Techniques for Accurate, Quantitative Immunohistochemistry

(2008) Simone P. Zehntner et al.   JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY