Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease
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[1] I. Módy,et al. Amyloid β induces interneuron-specific changes in the hippocampus of APPNL-F mice , 2020, PloS one.
[2] H. Nishimaru,et al. Astaxanthin Ameliorated Parvalbumin-Positive Neuron Deficits and Alzheimer’s Disease-Related Pathological Progression in the Hippocampus of AppNL-G-F/NL-G-F Mice , 2020, Frontiers in Pharmacology.
[3] R. J. McDonald,et al. Age-dependent behavioral and biochemical characterization of single APP knock-in mouse (APPNL-G-F/NL-G-F) model of Alzheimer's disease , 2019, Neurobiology of Aging.
[4] I. Vertkin,et al. Secreted amyloid-β precursor protein functions as a GABABR1a ligand to modulate synaptic transmission , 2019, Science.
[5] R. D'Hooge,et al. Subtle behavioral changes and increased prefrontal-hippocampal network synchronicity in APPNL−G−F mice before prominent plaque deposition , 2017, Behavioural Brain Research.
[6] M. Whittington,et al. Insoluble Aβ overexpression in an App knock-in mouse model alters microstructure and gamma oscillations in the prefrontal cortex, and social and anxiety-related behaviours , 2018, bioRxiv.
[7] R. D'Hooge,et al. Increased Insoluble Amyloid-β Induces Negligible Cognitive Deficits in Old AppNL/NL Knock-In Mice , 2018, Journal of Alzheimer's disease : JAD.
[8] T. Saido,et al. Neuroinflammation in mouse models of Alzheimer's disease , 2018, Clinical & experimental neuroimmunology.
[9] Jürgen Götz,et al. Rodent models for Alzheimer disease , 2018, Nature Reviews Neuroscience.
[10] T. Saido,et al. Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis , 2018, BMC Neuroscience.
[11] K. Fukunaga,et al. The Disease-modifying Drug Candidate, SAK3 Improves Cognitive Impairment and Inhibits Amyloid beta Deposition in App Knock-in Mice , 2018, Neuroscience.
[12] R. D'Hooge,et al. Spatial reversal learning defect coincides with hypersynchronous telencephalic BOLD functional connectivity in APPNL-F/NL-F knock-in mice , 2018, Scientific Reports.
[13] T. Saido,et al. Reduction in open field activity in the absence of memory deficits in the App NL−G−F knock-in mouse model of Alzheimer’s disease , 2018, Behavioural Brain Research.
[14] Hui Zheng,et al. Practical considerations for choosing a mouse model of Alzheimer’s disease , 2017, Molecular Neurodegeneration.
[15] B. Winblad,et al. APP mouse models for Alzheimer's disease preclinical studies , 2017, The EMBO journal.
[16] Y. Louzoun,et al. Corrigendum to “Unraveling cognitive traits using the Morris water maze unbiased strategy classification (MUST-C) algorithm” [Brain Behav. Immun. 52C (2016) 132–144] , 2017, Brain, Behavior, and Immunity.
[17] S. Itohara,et al. Cognitive deficits in single App knock-in mouse models , 2016, Neurobiology of Learning and Memory.
[18] Tomer Illouz,et al. Unraveling cognitive traits using the Morris water maze unbiased strategy classification (MUST-C) algorithm , 2016, Brain, Behavior, and Immunity.
[19] R. J. McDonald,et al. Barriers to developing a valid rodent model of Alzheimer's disease: from behavioral analysis to etiological mechanisms , 2015, Front. Neurosci..
[20] A. Palmeri,et al. Rodent models for Alzheimer’s disease drug discovery , 2015, Expert opinion on drug discovery.
[21] Rebecca Burwell,et al. Severity of spatial learning impairment in aging: Development of a learning index for performance in the Morris water maze. , 1993, Behavioral neuroscience.
[22] R. Hammer,et al. Vascular and parenchymal amyloid pathology in an Alzheimer disease knock-in mouse model: interplay with cerebral blood flow , 2014, Molecular Neurodegeneration.
[23] S. Itohara,et al. Single App knock-in mouse models of Alzheimer's disease , 2014, Nature Neuroscience.
[24] F. Schmitt,et al. Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models , 2014, Front. Genet..
[25] M. Savić,et al. Midazolam impairs acquisition and retrieval, but not consolidation of reference memory in the Morris water maze , 2013, Behavioural Brain Research.
[26] Robert Lalonde,et al. APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD) , 2012, Neuroscience & Biobehavioral Reviews.
[27] F. LaFerla,et al. Transgenic mouse models of Alzheimer disease: developing a better model as a tool for therapeutic interventions. , 2012, Current pharmaceutical design.
[28] Gianluigi Forloni,et al. APP Transgenic Mice: Their Use and Limitations , 2011, NeuroMolecular Medicine.
[29] Paul W. Frankland,et al. Frontiers in Integrative Neuroscience Integrative Neuroscience , 2022 .
[30] M. Ohno,et al. Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation , 2006, The Journal of Neuroscience.
[31] Hartwig Wolburg,et al. Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology , 2006, EMBO reports.
[32] H. Schröder,et al. Alzheimer's disease-like neuropathology of gene-targeted APP-SLxPS1mut mice expressing the amyloid precursor protein at endogenous levels , 2005, Neurobiology of Disease.
[33] Joanna L. Jankowsky,et al. Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase , 2004 .
[34] D. Borchelt,et al. Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase. , 2004, Human molecular genetics.
[35] B. Strooper,et al. FAD mutant PS-1 gene-targeted mice: increased Aβ42 and Aβ deposition without APP overproduction , 2002, Neurobiology of Aging.
[36] B. de Strooper,et al. FAD mutant PS-1 gene-targeted mice: increased A beta 42 and A beta deposition without APP overproduction. , 2002, Neurobiology of aging.
[37] D. Flood,et al. Presenilin-1 P264L Knock-In Mutation: Differential Effects on Aβ Production, Amyloid Deposition, and Neuronal Vulnerability , 2000, The Journal of Neuroscience.
[38] Miles W. Miller,et al. Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice , 1999, Nature Medicine.
[39] B. Sommer,et al. Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[40] S. Younkin,et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.
[41] B. Greenberg,et al. Enhanced Amyloidogenic Processing of the β-Amyloid Precursor Protein in Gene-targeted Mice Bearing the Swedish Familial Alzheimer's Disease Mutations and a “Humanized” Aβ Sequence* , 1996, The Journal of Biological Chemistry.
[42] L. Mucke,et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.
[43] M. Gallagher,et al. Severity of spatial learning impairment in aging: development of a learning index for performance in the Morris water maze. , 1993, Behavioral neuroscience.