Associated Papers
A C. elegans model of familial Alzheimer's disease shows age-dependent synaptic degeneration independent of amyloid β-peptide.
Nagarajan V et al.
Neurobiology of Disease, 2026
Dual Targeting of Tau Kinases and Autophagy by Abemaciclib Independent of CDK4/6 Inhibition.
Han J et al.
Advanced Science (weinheim, Baden-wurttemberg, Germany), 2026
Phenotypic variability in early-onset dementia segregating with a novel APP (p.I718M) variant.
Johansson C et al.
Alzheimer's Research & Therapy, 2025
A decade progress in the phenotyping of AppNL-G-F knock-in mouse model of Alzheimer's disease.
Manabe T et al.
Neuroscience Research, 2025
The landscape of autosomal-dominant Alzheimer's disease: global distribution and age of onset.
Liu H et al.
Brain : a Journal of Neurology, 2025
The Role of Neprilysin and Insulin-Degrading Enzyme in the Etiology of Sporadic Alzheimer's Disease.
Morito T et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2025
Spectrum of γ-Secretase dysfunction as a unifying predictor of ADAD age at onset across PSEN1, PSEN2 and APP causal genes.
Fernández SG et al.
Molecular Neurodegeneration, 2025
A Novel APP Knock-In Mouse Model to Study the Protective Effects of the Icelandic Mutation In Vivo.
Valle ML
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2025
Astrocytic centrin-2 expression in entorhinal cortex correlates with Alzheimer's disease severity.
Degl'Innocenti E et al.
Glia, 2024
The Icelandic Mutation (APP-A673T) Is Protective against Amyloid Pathology In Vivo.
Shimohama S et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2024
Microglia Gravitate toward Amyloid Plaques Surrounded by Externalized Phosphatidylserine via TREM2.
Park JC et al.
Advanced Science (weinheim, Baden-wurttemberg, Germany), 2024
Complement C3aR signaling: Immune and metabolic modulation and its impact on Alzheimer's disease.
Gedam M et al.
European Journal of Immunology, 2024
Apolipoprotein E polymorphisms and female fertility in a transgenic mouse model of Alzheimer's disease.
Medegan Fagla B et al.
Scientific Reports, 2024
Neuronal glutathione depletion elevates the Aβ42/Aβ40 ratio and tau aggregation in Alzheimer's disease mice.
Hashim KNB et al.
Febs Letters, 2024
Molecular mechanism of substrate recognition and cleavage by human γ-secretase.
Guo X et al.
Science (new York, N.y.), 2024
Divergent Age-Dependent Conformational Rearrangement within Aβ Amyloid Deposits in APP23, APPPS1, and AppNL-F Mice.
Parvin F et al.
Acs Chemical Neuroscience, 2024
Temporal Alterations in White Matter in An App Knock-In Mouse Model of Alzheimer's Disease.
Morrissey ZD et al.
Eneuro, 2024
The fluorescent ligand bTVBT2 reveals increased p-tau uptake by retinal microglia in Alzheimer's disease patients and AppNL-F/NL-F mice.
Nuñez-Diaz C et al.
Alzheimer's Research & Therapy, 2024
An Insertion Within SIRPβ1 Shows a Dual Effect Over Alzheimer's Disease Cognitive Decline Altering the Microglial Response.
García-Alberca JM et al.
Journal of Alzheimer's Disease : Jad, 2024
Early Astrocytic Dysfunction Is Associated with Mistuned Synapses as well as Anxiety and Depressive-Like Behavior in the AppNL-F Mouse Model of Alzheimer's Disease.
Portal B et al.
Journal of Alzheimer's Disease : Jad, 2024
Molecular pathology of neurodegenerative diseases by cryo-EM of amyloids.
Scheres SHW et al.
Nature, 2023
Mitochondrial hypermetabolism precedes impaired autophagy and synaptic disorganization in App knock-in Alzheimer mouse models.
Naia L et al.
Molecular Psychiatry, 2023
Differential effects of familial Alzheimer's disease-causing mutations on amyloid precursor protein (APP) trafficking, proteolytic conversion, and synaptogenic activity.
Schilling S et al.
Acta Neuropathologica Communications, 2023
Cryo-EM structures of amyloid-β filaments with the Arctic mutation (E22G) from human and mouse brains.
Yang Y et al.
Acta Neuropathologica, 2023
Specific Mutations near the Amyloid Precursor Protein Cleavage Site Increase γ-Secretase Sensitivity and Modulate Amyloid-β Production.
Suzuki R et al.
International Journal of Molecular Sciences, 2023
Amyloid precursor protein 𝛽CTF accumulates in synapses in sporadic and genetic forms of Alzheimer's disease.
Ferrer-Raventós P et al.
Neuropathology and Applied Neurobiology, 2023
Rare Amyloid Precursor Protein Point Mutations Recapitulate Worldwide Migration and Admixture in Healthy Individuals: Implications for the Study of Neurodegeneration.
Abondio P et al.
International Journal of Molecular Sciences, 2022
APP Knock-In Mice Produce E22P-Aβ Exhibiting an Alzheimer's Disease-like Phenotype with Dysregulation of Hypoxia-Inducible Factor Expression.
Maki T et al.
International Journal of Molecular Sciences, 2022
An isogenic panel of App knock-in mouse models: Profiling β-secretase inhibition and endosomal abnormalities.
Watamura N et al.
Science Advances, 2022
Somatostatin-evoked Aβ catabolism in the brain: Mechanistic involvement of α-endosulfine-KATP channel pathway.
Watamura N et al.
Molecular Psychiatry, 2022
Cryo-EM structures of amyloid-β 42 filaments from human brains.
Yang Y et al.
Science (new York, N.y.), 2022
Age-Dependent Behavioral and Metabolic Assessment of App NL-G-F/NL-G-F Knock-in (KI) Mice.
Wang S et al.
Frontiers in Molecular Neuroscience, 2022
Clinical characteristics and genotype-phenotype correlation analysis of familial Alzheimer's disease patients with pathogenic/likely pathogenic amyloid protein precursor mutations.
Liu Y et al.
Frontiers in Aging Neuroscience, 2022
Conformational Models of APP Processing by Gamma Secretase Based on Analysis of Pathogenic Mutations.
Kim M et al.
International Journal of Molecular Sciences, 2021
Τhe Greek Variant in APP Gene: The Phenotypic Spectrum of APP Mutations.
Kalampokini S et al.
International Journal of Molecular Sciences, 2021
Stem cell-derived neurons reflect features of protein networks, neuropathology, and cognitive outcome of their aged human donors.
Lagomarsino VN et al.
Neuron, 2021
Cerebral Small Vessel Disease in Sporadic and Familial Alzheimer Disease.
Kalaria RN et al.
The American Journal of Pathology, 2021
HMGB1 signaling phosphorylates Ku70 and impairs DNA damage repair in Alzheimer's disease pathology.
Tanaka H et al.
Communications Biology, 2021
Impaired spike-gamma coupling of area CA3 fast-spiking interneurons as the earliest functional impairment in the AppNL-G-F mouse model of Alzheimer's disease.
Arroyo-García LE et al.
Molecular Psychiatry, 2021
Spreading of Alzheimer tau seeds is enhanced by aging and template matching with limited impact of amyloid-β.
Nies SH et al.
The Journal of Biological Chemistry, 2021
A third-generation mouse model of Alzheimer's disease shows early and increased cored plaque pathology composed of wild-type human amyloid β peptide.
Sato K et al.
The Journal of Biological Chemistry, 2021
Prediction and verification of the AD-FTLD common pathomechanism based on dynamic molecular network analysis.
Jin M et al.
Communications Biology, 2021
Aβ43 aggregates exhibit enhanced prion-like seeding activity in mice.
Ruiz-Riquelme A et al.
Acta Neuropathologica Communications, 2021
Pulse-Chase Proteomics of the App Knockin Mouse Models of Alzheimer's Disease Reveals that Synaptic Dysfunction Originates in Presynaptic Terminals.
Hark TJ et al.
Cell Systems, 2021
Amyloid Β-Peptide Increases Mitochondria-Endoplasmic Reticulum Contact Altering Mitochondrial Function and Autophagosome Formation in Alzheimer's Disease-Related Models.
Leal NS et al.
Cells, 2020
Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in.
Chiasseu M et al.
Neurobiology of Disease, 2020
Modeling the β-secretase cleavage site and humanizing amyloid-beta precursor protein in rat and mouse to study Alzheimer's disease.
Serneels L et al.
Molecular Neurodegeneration, 2020
Amyloidosis is associated with thicker myelin and increased oligodendrogenesis in the adult mouse brain.
Ferreira S et al.
Journal of Neuroscience Research, 2020