Pages that link to "Q36037957"
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The following pages link to β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia (Q36037957):
Displaying 50 items.
- Precocious Alterations of Brain Oscillatory Activity in Alzheimer's Disease: A Window of Opportunity for Early Diagnosis and Treatment (Q26770751) (← links)
- A γ-secretase inhibitor, but not a γ-secretase modulator, induced defects in BDNF axonal trafficking and signaling: evidence for a role for APP (Q27314017) (← links)
- Dynamin 1 regulates amyloid generation through modulation of BACE-1 (Q27318742) (← links)
- Amyloid precursor protein-mediated endocytic pathway disruption induces axonal dysfunction and neurodegeneration (Q27331605) (← links)
- Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer's disease mouse model (Q28247764) (← links)
- 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 functions (Q28543167) (← links)
- Deletion of the γ-secretase subunits Aph1B/C impairs memory and worsens the deficits of knock-in mice modeling the Alzheimer-like familial Danish dementia (Q28600984) (← links)
- Ligand-dependent activation of EphA4 signaling regulates the proteolysis of amyloid precursor protein through a Lyn-mediated pathway (Q31814817) (← links)
- Lysosomal dysfunction in the brain of a mouse model with intraneuronal accumulation of carboxyl terminal fragments of the amyloid precursor protein (Q33603071) (← links)
- 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 (Q34477111) (← links)
- An intracellular threonine of amyloid-β precursor protein mediates synaptic plasticity deficits and memory loss (Q34603033) (← links)
- Early hyperactivity in lateral entorhinal cortex is associated with elevated levels of AβPP metabolites in the Tg2576 mouse model of Alzheimer's disease. (Q35071690) (← links)
- Specific antibody binding to the APP672-699 region shifts APP processing from α- to β-cleavage (Q35679539) (← links)
- Memory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency. (Q35917231) (← links)
- Lessons from a Rare Familial Dementia: Amyloid and Beyond (Q36082628) (← links)
- Effects of BACE1 haploinsufficiency on APP processing and Aβ concentrations in male and female 5XFAD Alzheimer mice at different disease stages (Q36113733) (← links)
- Inhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia (Q36124692) (← links)
- Tyr682 in the Aβ-precursor protein intracellular domain regulates synaptic connectivity, cholinergic function, and cognitive performance (Q36405899) (← links)
- The exosome secretory pathway transports amyloid precursor protein carboxyl-terminal fragments from the cell into the brain extracellular space (Q36466825) (← links)
- Evidence that the rab5 effector APPL1 mediates APP-βCTF-induced dysfunction of endosomes in Down syndrome and Alzheimer's disease (Q36488014) (← links)
- Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection (Q36526897) (← links)
- APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses (Q36585916) (← links)
- Amyloid plaque pathogenesis in 5XFAD mouse spinal cord: retrograde transneuronal modulation after peripheral nerve injury (Q36586319) (← links)
- Partial BACE1 reduction in a Down syndrome mouse model blocks Alzheimer-related endosomal anomalies and cholinergic neurodegeneration: role of APP-CTF. (Q36638747) (← links)
- Normal cognition in transgenic BRI2-Aβ mice (Q36858817) (← links)
- Interaction of ApoE3 and ApoE4 isoforms with an ITM2b/BRI2 mutation linked to the Alzheimer disease-like Danish dementia: Effects on learning and memory (Q36988218) (← links)
- Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis (Q37013605) (← links)
- Intraneuronal aggregation of the β-CTF fragment of APP (C99) induces Aβ-independent lysosomal-autophagic pathology. (Q37099349) (← links)
- Increased expression of reticulon 3 in neurons leads to reduced axonal transport of β site amyloid precursor protein-cleaving enzyme 1. (Q37234006) (← links)
- Phenotypic Alterations in Hippocampal NPY- and PV-Expressing Interneurons in a Presymptomatic Transgenic Mouse Model of Alzheimer's Disease. (Q37592706) (← links)
- Differential contribution of APP metabolites to early cognitive deficits in a TgCRND8 mouse model of Alzheimer's disease (Q37665855) (← links)
- Amyloid β-protein oligomers and Alzheimer's disease (Q37690332) (← links)
- Exosomes in the Diseased Brain: First Insights from In vivo Studies (Q37716769) (← links)
- Targeting synaptic dysfunction in Alzheimer's disease therapy. (Q38036916) (← links)
- Yeast Model of Amyloid-β and Tau Aggregation in Alzheimer's Disease (Q38592263) (← links)
- Abolishing Tau cleavage by caspases at Aspartate421 causes memory/synaptic plasticity deficits and pre-pathological Tau alterations (Q38634954) (← links)
- A Greek Tragedy: The Growing Complexity of Alzheimer Amyloid Precursor Protein Proteolysis (Q38913292) (← links)
- The ITM2B (BRI2) gene is a target of BCL6 repression: Implications for lymphomas and neurodegenerative diseases (Q38923425) (← links)
- Not just amyloid: physiological functions of the amyloid precursor protein family (Q39209681) (← links)
- Transthyretin and BRICHOS: The Paradox of Amyloidogenic Proteins with Anti-Amyloidogenic Activity for Aβ in the Central Nervous System (Q39209937) (← links)
- Amyloid precursor protein and endosomal-lysosomal dysfunction in Alzheimer's disease: inseparable partners in a multifactorial disease (Q39405747) (← links)
- Sex-related dimorphism in dentate gyrus atrophy and behavioral phenotypes in an inducible tTa:APPsi transgenic model of Alzheimer's disease. (Q39445728) (← links)
- Amyloid Precursor Protein (APP) May Act as a Substrate and a Recognition Unit for CRL4CRBN and Stub1 E3 Ligases Facilitating Ubiquitination of Proteins Involved in Presynaptic Functions and Neurodegeneration (Q41045804) (← links)
- Inactivation of γ-secretases leads to accumulation of substrates and non-Alzheimer neurodegeneration (Q41198109) (← links)
- Role of BACE1 in Alzheimer's synaptic function. (Q41555225) (← links)
- Molecular mechanisms of Alzheimer disease protection by the A673T allele of amyloid precursor protein (Q41788034) (← links)
- RETRACTED: Elevation of brain magnesium prevents and reverses cognitive deficits and synaptic loss in Alzheimer's disease mouse model. (Q44968491) (← links)
- Alterations in hippocampal network oscillations and theta-gamma coupling arise before Aβ overproduction in a mouse model of Alzheimer's disease (Q45344473) (← links)
- Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease (Q47149447) (← links)
- Human Brain-Derived Aβ Oligomers Bind to Synapses and Disrupt Synaptic Activity in a Manner That Requires APP. (Q47443049) (← links)