β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia.
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Precocious Alterations of Brain Oscillatory Activity in Alzheimer's Disease: A Window of Opportunity for Early Diagnosis and TreatmentA γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APPDynamin 1 regulates amyloid generation through modulation of BACE-1Amyloid precursor protein-mediated endocytic pathway disruption induces axonal dysfunction and neurodegenerationElevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer's disease mouse model.APP is cleaved by Bace1 in pre-synaptic vesicles and establishes a pre-synaptic interactome, via its intracellular domain, with molecular complexes that regulate pre-synaptic vesicles functionsDeletion of the γ-secretase subunits Aph1B/C impairs memory and worsens the deficits of knock-in mice modeling the Alzheimer-like familial Danish dementiaLigand-dependent activation of EphA4 signaling regulates the proteolysis of amyloid precursor protein through a Lyn-mediated pathway.Lysosomal dysfunction in the brain of a mouse model with intraneuronal accumulation of carboxyl terminal fragments of the amyloid precursor protein.The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus.An intracellular threonine of amyloid-β precursor protein mediates synaptic plasticity deficits and memory loss.Early hyperactivity in lateral entorhinal cortex is associated with elevated levels of AβPP metabolites in the Tg2576 mouse model of Alzheimer's disease.Specific antibody binding to the APP672-699 region shifts APP processing from α- to β-cleavageMemory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency.Lessons from a Rare Familial Dementia: Amyloid and Beyond.Effects of BACE1 haploinsufficiency on APP processing and Aβ concentrations in male and female 5XFAD Alzheimer mice at different disease stagesInhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia.Tyr682 in the Aβ-precursor protein intracellular domain regulates synaptic connectivity, cholinergic function, and cognitive performance.The exosome secretory pathway transports amyloid precursor protein carboxyl-terminal fragments from the cell into the brain extracellular space.Evidence that the rab5 effector APPL1 mediates APP-βCTF-induced dysfunction of endosomes in Down syndrome and Alzheimer's disease.Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection.APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses.Amyloid plaque pathogenesis in 5XFAD mouse spinal cord: retrograde transneuronal modulation after peripheral nerve injuryPartial BACE1 reduction in a Down syndrome mouse model blocks Alzheimer-related endosomal anomalies and cholinergic neurodegeneration: role of APP-CTF.Normal cognition in transgenic BRI2-Aβ mice.Interaction of ApoE3 and ApoE4 isoforms with an ITM2b/BRI2 mutation linked to the Alzheimer disease-like Danish dementia: Effects on learning and memoryReversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis.Intraneuronal aggregation of the β-CTF fragment of APP (C99) induces Aβ-independent lysosomal-autophagic pathology.Increased expression of reticulon 3 in neurons leads to reduced axonal transport of β site amyloid precursor protein-cleaving enzyme 1.Phenotypic Alterations in Hippocampal NPY- and PV-Expressing Interneurons in a Presymptomatic Transgenic Mouse Model of Alzheimer's Disease.Differential contribution of APP metabolites to early cognitive deficits in a TgCRND8 mouse model of Alzheimer's disease.Amyloid β-protein oligomers and Alzheimer's disease.Exosomes in the Diseased Brain: First Insights from In vivo Studies.Targeting synaptic dysfunction in Alzheimer's disease therapy.Yeast Model of Amyloid-β and Tau Aggregation in Alzheimer's Disease.Abolishing Tau cleavage by caspases at Aspartate421 causes memory/synaptic plasticity deficits and pre-pathological Tau alterations.A Greek Tragedy: The Growing Complexity of Alzheimer Amyloid Precursor Protein Proteolysis.The ITM2B (BRI2) gene is a target of BCL6 repression: Implications for lymphomas and neurodegenerative diseases.Not just amyloid: physiological functions of the amyloid precursor protein family.Transthyretin and BRICHOS: The Paradox of Amyloidogenic Proteins with Anti-Amyloidogenic Activity for Aβ in the Central Nervous System.
P2860
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P2860
β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
β- but not γ-secretase proteol ...... in a mouse model of dementia.
@ast
β- but not γ-secretase proteol ...... in a mouse model of dementia.
@en
type
label
β- but not γ-secretase proteol ...... in a mouse model of dementia.
@ast
β- but not γ-secretase proteol ...... in a mouse model of dementia.
@en
prefLabel
β- but not γ-secretase proteol ...... in a mouse model of dementia.
@ast
β- but not γ-secretase proteol ...... in a mouse model of dementia.
@en
P2860
P50
P356
P1476
β- but not γ-secretase proteol ...... in a mouse model of dementia.
@en
P2093
Robert Tamayev
Shuji Matsuda
P2860
P304
P356
10.1002/EMMM.201100195
P577
2012-01-23T00:00:00Z