ER stress is not elevated in the 5XFAD mouse model of Alzheimer's disease

Endoplasmic reticulum stress responses in mouse models of Alzheimer's disease: Overexpression paradigmversusknockin paradigm

(2018) Shoko Hashimoto et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Emerging roles of ER stress in the etiology and pathogenesis of Alzheimer's disease

(2017) Yannis Gerakis et al.   FEBS Journal

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

(2016) Inger Lauritzen et al.   ACTA NEUROPATHOLOGICA

The amyloid hypothesis of Alzheimer's disease at 25 years

(2016) Dennis J Selkoe et al.   EMBO Molecular Medicine

Calpain Activation in Alzheimer's Model Mice Is an Artifact of APP and Presenilin Overexpression

(2016) T. Saito et al.   JOURNAL OF NEUROSCIENCE

The transcription factor XBP1s restores hippocampal synaptic plasticity and memory by control of the Kalirin-7 pathway in Alzheimer model

(2016) M Cissé et al.   MOLECULAR PSYCHIATRY

The unfolded protein response in neurodegenerative diseases: a neuropathological perspective

(2015) Wiep Scheper et al.   ACTA NEUROPATHOLOGICA

Aβ reduction in BACE1 heterozygous null 5XFAD mice is associated with transgenic APP level

(2015) Katherine R Sadleir et al.   Molecular Neurodegeneration

Evidence that the rab5 effector APPL1 mediates APP-βCTF-induced dysfunction of endosomes in Down syndrome and Alzheimer’s disease

(2015) S Kim et al.   MOLECULAR PSYCHIATRY

Single App knock-in mouse models of Alzheimer's disease

(2014) Takashi Saito et al.   NATURE NEUROSCIENCE

PERK mediates eIF2α phosphorylation responsible for BACE1 elevation, CREB dysfunction and neurodegeneration in a mouse model of Alzheimer's disease

(2014) Latha Devi et al.   NEUROBIOLOGY OF AGING

Granulovacuolar degeneration and unfolded protein response in mouse models of tauopathy and Aβ amyloidosis

(2014) Christoph Köhler et al.   NEUROBIOLOGY OF DISEASE

Genetic Inhibition of Phosphorylation of the Translation Initiation Factor eIF2α Does Not Block Aβ-Dependent Elevation of BACE1 and APP Levels or Reduce Amyloid Pathology in a Mouse Model of Alzheimer’s Disease

(2014) Katherine R. Sadleir et al.   PLoS One

Elevated Aβ42 in Aged, Non-demented Individuals with Cerebral Atherosclerosis

(2013) Katherine Sadleir et al.   Current Alzheimer Research

Neuron loss in the 5XFAD mouse model of Alzheimer’s disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation

(2013) William A Eimer et al.   Molecular Neurodegeneration

Deletion of the eIF2α Kinase GCN2 Fails to Rescue the Memory Decline Associated with Alzheimer’s Disease

(2013) Latha Devi et al.   PLoS One

The Genetics of Alzheimer Disease

(2013) R. E. Tanzi   Cold Spring Harbor Perspectives in Medicine

Mechanisms that lessen benefits of β-secretase reduction in a mouse model of Alzheimer’s disease

(2013) L Devi et al.   Translational Psychiatry

Signaling Pathways from the Endoplasmic Reticulum and Their Roles in Disease

(2013) Hisae Kadowaki et al.   Genes

The unfolded protein response is activated in disease-affected brain regions in progressive supranuclear palsy and Alzheimer’s disease

(2013) Lauren D Stutzbach et al.   Acta Neuropathologica Communications

Enhanced  -secretase processing alters APP axonal transport and leads to axonal defects

(2012) E. M. Rodrigues et al.   HUMAN MOLECULAR GENETICS

Activation of the Unfolded Protein Response Is an Early Event in Alzheimer’s and Parkinson’s Disease

(2012) Jeroen J.M. Hoozemans et al.   Neurodegenerative Diseases

The unfolded protein response is associated with early tau pathology in the hippocampus of tauopathies

(2011) Diana AT Nijholt et al.   JOURNAL OF PATHOLOGY

Phospho-eIF2α Level Is Important for Determining Abilities of BACE1 Reduction to Rescue Cholinergic Neurodegeneration and Memory Defects in 5XFAD Mice

(2010) Latha Devi et al.   PLoS One

The Unfolded Protein Response Is Activated in Pretangle Neurons in Alzheimer's Disease Hippocampus

(2009) Jeroen J.M. Hoozemans et al.   AMERICAN JOURNAL OF PATHOLOGY

Phosphorylation of the Translation Initiation Factor eIF2α Increases BACE1 Levels and Promotes Amyloidogenesis

(2008) Tracy O'Connor et al.   NEURON