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Tau is not necessary for amyloid-β-induced synaptic and memory impairments.
- Published in:
- 2020
- By:
- Publication type:
- journal article
Analysis of early effects of human APOE isoforms on Alzheimer's disease and type III hyperlipoproteinemia pathways using knock-in rat models with humanized APP and APOE.
- Published in:
- Cell Communication & Signaling, 2024, v. 22, n. 1, p. 1, doi. 10.1186/s12964-024-01832-2
- By:
- Publication type:
- Article
Functional BRI2-TREM2 interactions in microglia: implications for Alzheimer's and related dementias.
- Published in:
- EMBO Reports, 2024, v. 25, n. 3, p. 1326, doi. 10.1038/s44319-024-00077-x
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- Publication type:
- Article
Significance of Blood and Cerebrospinal Fluid Biomarkers for Alzheimer's Disease: Sensitivity, Specificity and Potential for Clinical Use.
- Published in:
- Journal of Personalized Medicine, 2020, v. 10, n. 3, p. 116, doi. 10.3390/jpm10030116
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- Publication type:
- Article
BRI2 Inhibits Amyloid β-Peptide Precursor Protein Processing by Interfering with the Docking of Secretases to the Substrate.
- Published in:
- Journal of Neuroscience, 2008, v. 28, n. 35, p. 8668, doi. 10.1523/JNEUROSCI.2094-08.2008
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- Publication type:
- Article
APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release.
- Published in:
- eLife, 2015, p. 1, doi. 10.7554/eLife.09743
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- Publication type:
- Article
Generation of mouse natural killer (NK) cell activity: Effect of interleukin-2 (IL-2) and interferon (IFN) on the in vivo development of natural killer cells from bone marrow (BM) progenitor cells.
- Published in:
- International Journal of Cancer, 1986, v. 38, n. 4, p. 553, doi. 10.1002/ijc.2910380416
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- Publication type:
- Article
APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant.
- Published in:
- EMBO Journal, 2011, v. 30, n. 12, p. 2501, doi. 10.1038/emboj.2011.161
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- Publication type:
- Article
Thymic and peripheral apoptosis of antigen-specific T cells might cooperate in establishing self tolerance.
- Published in:
- European Journal of Immunology, 1993, v. 23, n. 3, p. 747, doi. 10.1002/eji.1830230327
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- Publication type:
- Article
β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia.
- Published in:
- EMBO Molecular Medicine, 2012, v. 4, n. 3, p. 171, doi. 10.1002/emmm.201100195
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- Publication type:
- Article
Initial assessment of the spatial learning, reversal, and sequencing task capabilities of knock-in rats with humanizing mutations in the Aβ-coding region of App.
- Published in:
- PLoS ONE, 2022, v. 17, n. 5, p. 1, doi. 10.1371/journal.pone.0263546
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- Publication type:
- Article
Facilitation of glutamate, but not GABA, release in Familial Alzheimer's APP mutant Knock‐in rats with increased β‐cleavage of APP.
- Published in:
- Aging Cell, 2019, v. 18, n. 6, p. N.PAG, doi. 10.1111/acel.13033
- By:
- Publication type:
- Article
Tyr682 in the Aβ-precursor protein intracellular domain regulates synaptic connectivity, cholinergic function, and cognitive performance.
- Published in:
- Aging Cell, 2012, v. 11, n. 6, p. 1084, doi. 10.1111/acel.12009
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- Publication type:
- Article
The Familial dementia gene ITM2b/BRI2 facilitates glutamate transmission via both presynaptic and postsynaptic mechanisms.
- Published in:
- Scientific Reports, 2019, v. 9, n. 1, p. 1, doi. 10.1038/s41598-019-41340-9
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- Publication type:
- Article
Regulation of Fas ligand expression and cell death by apoptosis-linked gene 4.
- Published in:
- Nature Medicine, 1999, v. 5, n. 5, p. 542, doi. 10.1038/8420
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- Publication type:
- Article
Increased AβPP Processing in Familial Danish Dementia Patients.
- Published in:
- Journal of Alzheimer's Disease, 2011, v. 27, n. 2, p. 385, doi. 10.3233/JAD-2011-110785
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- Publication type:
- Article
Increased AβPP processing in familial Danish dementia patients.
- Published in:
- 2011
- By:
- Publication type:
- journal article
Phosphorylation of a tyrosine in the amyloid-beta protein precursor intracellular domain inhibits Fe65 binding and signaling.
- Published in:
- 2009
- By:
- Publication type:
- journal article
Phosphorylation of a Tyrosine in the Amyloid-β Protein Precursor Intracellular Domain Inhibits Fe65 Binding and Signaling.
- Published in:
- Journal of Alzheimer's Disease, 2009, v. 16, n. 2, p. 301, doi. 10.3233/JAD-2009-0970
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- Publication type:
- Article
The intracellular localization of amyloid beta protein precursor (AbetaPP) intracellular domain associated protein-1 (AIDA-1) is regulated by AbetaPP and alternative splicing.
- Published in:
- 2004
- By:
- Publication type:
- journal article
The intracellular localization of amyloid β protein precursor (AβPP) intracellular domain associated protein-1 (AIDA-1) is regulated by AβPP and alternative splicing.
- Published in:
- Journal of Alzheimer's Disease, 2004, v. 6, n. 1, p. 67, doi. 10.3233/JAD-2004-6108
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- Publication type:
- Article
Neuronal apoptosis is accompanied by amyloid beta-protein accumulation in the endoplasmic reticulum.
- Published in:
- 2002
- By:
- Publication type:
- journal article
Neuronal apoptosis is accompanied by amyloid β-protein accumulation in the endoplasmic reticulum.
- Published in:
- Journal of Alzheimer's Disease, 2002, v. 4, n. 1, p. 31, doi. 10.3233/JAD-2002-4104
- By:
- Publication type:
- Article
Correction: Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade.
- Published in:
- 2024
- By:
- Publication type:
- Correction Notice
Late-long-term potentiation magnitude, but not Ab levels and amyloid pathology, is associated with behavioral performance in a rat knock-in model of Alzheimer disease.
- Published in:
- Frontiers in Aging Neuroscience, 2022, v. 14, p. 1, doi. 10.3389/fnagi.2022.1040576
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- Publication type:
- Article
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.
- Published in:
- PLoS ONE, 2014, v. 9, n. 9, p. 1, doi. 10.1371/journal.pone.0108576
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- Publication type:
- Article
An Intracellular Threonine of Amyloid-β Precursor Protein Mediates Synaptic Plasticity Deficits and Memory Loss.
- Published in:
- PLoS ONE, 2013, v. 8, n. 2, p. 1, doi. 10.1371/journal.pone.0057120
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- Publication type:
- Article
The Intracellular Threonine of Amyloid Precursor Protein That Is Essential for Docking of Pin1 Is Dispensable for Developmental Function.
- Published in:
- PLoS ONE, 2011, v. 6, n. 3, p. 1, doi. 10.1371/journal.pone.0018006
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- Publication type:
- Article
Tyr<sup>682</sup> in the Intracellular Domain of APP Regulates Amyloidogenic APP Processing In Vivo.
- Published in:
- PLoS ONE, 2010, v. 5, n. 11, p. 1, doi. 10.1371/journal.pone.0015503
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- Publication type:
- Article
Transgenic Expression of the Amyloid-β Precursor Protein-Intracellular Domain Does Not Induce Alzheimer's Disease--Like Traits In Vivo.
- Published in:
- PLoS ONE, 2010, v. 5, n. 7, p. 1, doi. 10.1371/journal.pone.0011609
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- Publication type:
- Article
Memory Deficits of British Dementia Knock-In Mice Are Prevented by A&bgr;-Precursor Protein Haploinsufficiency.
- Published in:
- Journal of Neuroscience, 2012, v. 32, n. 16, p. 5481, doi. 10.1523/JNEUROSCI.5193-11.2012
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- Publication type:
- Article
APP is Phosphorylated by TrkA and Regulates NGF/TrkA Signaling.
- Published in:
- Journal of Neuroscience, 2011, v. 31, n. 33, p. 11756, doi. 10.1523/JNEUROSCI.1960-11.2011
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- Publication type:
- Article
Memory Deficits Due to Familial British Dementia BRI2 Mutation Are Caused by Loss of BRI2 Function Rather than Amyloidosis.
- Published in:
- Journal of Neuroscience, 2010, v. 30, n. 44, p. 14915, doi. 10.1523/JNEUROSCI.3917-10.2010
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- Publication type:
- Article
APP/AICD‐dependent expression of Glypican 4 mediates accumulation of tau oligomers in astrocytes and their synaptotoxic action.
- Published in:
- Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 2023, v. 19, p. 1, doi. 10.1002/alz.075708
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- Publication type:
- Article
PRESYNAPTIC AMYLOID PRECURSOR PROTEIN IS NECESSARY FOR THE IMPAIRMENT OF SYNAPTIC FUNCTION AND MEMORY CAUSED BY EXTRACELLULAR AMYLOID‐ΒETA AND TAU OLIGOMERS.
- Published in:
- Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 2023, v. 19, p. 1, doi. 10.1002/alz.075844
- By:
- Publication type:
- Article
APP/AICD‐dependent expression of Glypican 4 mediates accumulation of tau oligomers in astrocytes and their synaptotoxic action.
- Published in:
- Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 2023, v. 19, p. 1, doi. 10.1002/alz.075708
- By:
- Publication type:
- Article
PRESYNAPTIC AMYLOID PRECURSOR PROTEIN IS NECESSARY FOR THE IMPAIRMENT OF SYNAPTIC FUNCTION AND MEMORY CAUSED BY EXTRACELLULAR AMYLOID‐ΒETA AND TAU OLIGOMERS.
- Published in:
- Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 2023, v. 19, p. 1, doi. 10.1002/alz.075844
- By:
- Publication type:
- Article
Tyr 682 on APP intracellular domain modulates NGF signaling
- Published in:
- 2011
- By:
- Publication type:
- Abstract
Do BRI2 mutations cause early onset Alzheimer's disease?
- Published in:
- 2010
- By:
- Publication type:
- Abstract
O3-03-01: Presenilin-dependent transcriptional control of the Aβ-degrading enzyme neprilysin by AICD
- Published in:
- 2006
- By:
- Publication type:
- Abstract
O1-02-04: Regulation of APP processing by the familial dementia gene BRI2
- Published in:
- 2006
- By:
- Publication type:
- Abstract
O3-03-01: Presenilin-dependent transcriptional control of the Aβ-degrading enzyme neprilysin by AICD
- Published in:
- 2006
- By:
- Publication type:
- Abstract
O1-02-04: Regulation of APP processing by the familial dementia gene BRI2
- Published in:
- 2006
- By:
- Publication type:
- Abstract
Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade.
- Published in:
- Molecular Neurodegeneration, 2019, v. 14, n. 1, p. N.PAG, doi. 10.1186/s13024-019-0326-4
- By:
- Publication type:
- Article
Tuning of Glutamate, But Not GABA, Release by an Intrasynaptic Vesicle APP Domain Whose Function Can Be Modulated by β- or α-Secretase Cleavage.
- Published in:
- Journal of Neuroscience, 2019, v. 39, n. 35, p. 6992, doi. 10.1523/JNEUROSCI.0207-19.2019
- By:
- Publication type:
- Article
Rescue of Learning and Memory Deficits in the Human Nonsyndromic Intellectual Disability Cereblon Knock-Out Mouse Model by Targeting the AMP-Activated Protein Kinase-mTORCl Translational Pathway.
- Published in:
- Journal of Neuroscience, 2018, v. 38, n. 11, p. 2780, doi. 10.1523/JNEUROSCI.0599-17.2018
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- Publication type:
- Article
Gadd45ß mediates the NF-?B suppression of JNK signalling by targeting MKK7/JNKK2.
- Published in:
- Nature Cell Biology, 2004, v. 6, n. 2, p. 146, doi. 10.1038/ncb1093
- By:
- Publication type:
- Article
Modeling familial British and Danish dementia.
- Published in:
- Brain Structure & Function, 2010, v. 214, n. 2/3, p. 235, doi. 10.1007/s00429-009-0221-9
- By:
- Publication type:
- Article
β - but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia.
- Published in:
- 2012
- By:
- Publication type:
- Abstract
Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection.
- Published in:
- Molecular Neurodegeneration, 2012, v. 7, n. 1, p. 60, doi. 10.1186/1750-1326-7-60
- By:
- Publication type:
- Article