APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
about
Ferulic acid is a nutraceutical β-secretase modulator that improves behavioral impairment and alzheimer-like pathology in transgenic miceA mouse model of Down syndrome trisomic for all human chromosome 21 syntenic regions.Gender-Specific Hippocampal Dysrhythmia and Aberrant Hippocampal and Cortical Excitability in the APPswePS1dE9 Model of Alzheimer's DiseaseEnvironmental novelty exacerbates stress hormones and Aβ pathology in an Alzheimer's model.A presenilin-1 mutation identified in familial Alzheimer disease with cotton wool plaques causes a nearly complete loss of gamma-secretase activityCalpain activation promotes BACE1 expression, amyloid precursor protein processing, and amyloid plaque formation in a transgenic mouse model of Alzheimer diseaseIdentification of amyloid plaques in retinas from Alzheimer's patients and noninvasive in vivo optical imaging of retinal plaques in a mouse model.Methylene blue modulates β-secretase, reverses cerebral amyloidosis, and improves cognition in transgenic mice.Induction of methionine-sulfoxide reductases protects neurons from amyloid β-protein insults in vitro and in vivo.Tannic acid is a natural β-secretase inhibitor that prevents cognitive impairment and mitigates Alzheimer-like pathology in transgenic mice.The Effect of a High-Fat Diet on Brain Plasticity, Inflammation and Cognition in Female ApoE4-Knockin and ApoE-Knockout MiceMotor Cortex Theta and Gamma Architecture in Young Adult APPswePS1dE9 Alzheimer Mice.Presenilin transgenic mice as models of Alzheimer's disease.Neurogenesis, Neurodegeneration, Interneuron Vulnerability, and Amyloid-β in the Olfactory Bulb of APP/PS1 Mouse Model of Alzheimer's Disease.An update of animal models of Alzheimer disease with a reevaluation of plaque depositions.The impact of Bdnf gene deficiency to the memory impairment and brain pathology of APPswe/PS1dE9 mouse model of Alzheimer's disease.Redundant Gs-coupled serotonin receptors regulate amyloid-β metabolism in vivo.Deletion of the type-1 interferon receptor in APPSWE/PS1ΔE9 mice preserves cognitive function and alters glial phenotypeAutophagy is involved in oligodendroglial precursor-mediated clearance of amyloid peptide.Interaction between amyloid-β pathology and cortical functional columnar organization.Outstanding Phenotypic Differences in the Profile of Amyloid-β between Tg2576 and APPswe/PS1dE9 Transgenic Mouse Models of Alzheimer's Disease.Generation of a new transgenic mouse model for assessment of tau gene silencing therapies.Expression of Phenotypic Astrocyte Marker Is Increased in a Transgenic Mouse Model of Alzheimer's Disease versus Age-Matched Controls: A Presymptomatic Stage Study.High plasticity of axonal pathology in Alzheimer's disease mouse models.Familial Alzheimer's disease-associated presenilin-1 alters cerebellar activity and calcium homeostasis.Mouse models of Alzheimer's disease.Animal models of neurodegenerative diseases.Combination therapy with octyl gallate and ferulic acid improves cognition and neurodegeneration in a transgenic mouse model of Alzheimer's disease.Progressive Neuronal Pathology and Synaptic Loss Induced by Prediabetes and Type 2 Diabetes in a Mouse Model of Alzheimer's Disease.Interference with splicing of Presenilin transcripts has potent dominant negative effects on Presenilin activity.Proteomic Analysis of Protein Expression Throughout Disease Progression in a Mouse Model of Alzheimer's Disease.An integrated proteomics approach shows synaptic plasticity changes in an APP/PS1 Alzheimer's mouse model.T cell mediated cerebral hemorrhages and microhemorrhages during passive Aβ immunization in APPPS1 transgenic mice.Accelerated neurodegeneration and neuroinflammation in transgenic mice expressing P301L tau mutant and tau-tubulin kinase 1.The diabetes drug liraglutide ameliorates aberrant insulin receptor localisation and signalling in parallel with decreasing both amyloid-β plaque and glial pathology in a mouse model of Alzheimer's disease.A reporter of local dendritic translocation shows plaque- related loss of neural system function in APP-transgenic mice.Enriched physical environment reverses spatial cognitive impairment of socially isolated APPswe/PS1dE9 transgenic mice before amyloidosis onset.Calmodulin-like skin protein protects against spatial learning impairment in a mouse model of Alzheimer disease.Chronic cannabidiol treatment improves social and object recognition in double transgenic APPswe/PS1∆E9 mice.Antioxidative and Anti-Apoptotic Roles of Silibinin in Reversing Learning and Memory Deficits in APP/PS1 Mice.
P2860
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P2860
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh-hant
name
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
@en
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
@nl
type
label
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
@en
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
@nl
prefLabel
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
@en
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
@nl
P2093
P1476
APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1.
@en
P2093
David R Borchelt
Hilda H Slunt
Joanna L Jankowsky
Victoria Gonzales
P304
P356
10.1016/J.NEUROBIOLAGING.2003.09.008
P577
2004-08-01T00:00:00Z