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APP Deletion Accounts for Age-Dependent Changes in the Bioenergetic Metabolism and in Hyperphosphorylated CaMKII at Stimulated Hippocampal Presynaptic Active Zones.
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- Frontiers in Synaptic Neuroscience, 2017, v. 9, p. 1, doi. 10.3389/fnsyn.2017.00001
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Editorial: The Physiological Functions of the APP Gene Family.
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- Frontiers in Molecular Neuroscience, 2017, p. 1, doi. 10.3389/fnmol.2017.00334
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Amyloid-precursor Like Proteins APLP1 and APLP2 Are Dispensable for Normal Development of the Neonatal Respiratory Network.
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- Frontiers in Molecular Neuroscience, 2017, p. 1, doi. 10.3389/fnmol.2017.00189
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Therapeutic Potential of Secreted Amyloid Precursor Protein APPsα.
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- Frontiers in Molecular Neuroscience, 2017, v. 10, p. 1, doi. 10.3389/fnmol.2017.00030
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Region-Specific Differences in Amyloid Precursor Protein Expression in the Mouse Hippocampus.
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- Frontiers in Molecular Neuroscience, 2016, v. 9, p. 1, doi. 10.3389/fnmol.2016.00134
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In vivo Ca<sup>2+</sup> imaging of astrocytic microdomains reveals a critical role of the amyloid precursor protein for mitochondria.
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- Glia, 2019, v. 67, n. 5, p. 985, doi. 10.1002/glia.23584
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- Article
APP family member dimeric complexes are formed predominantly in synaptic compartments.
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- Cell & Bioscience, 2023, v. 13, n. 1, p. 1, doi. 10.1186/s13578-023-01092-6
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Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism‐like phenotype.
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- EMBO Journal, 2021, v. 40, n. 12, p. 1, doi. 10.15252/embj.2020107471
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Specific gene transfer to neurons, endothelial cells and hematopoietic progenitors with lentiviral vectors.
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- Nature Methods, 2010, v. 7, n. 11, p. 929, doi. 10.1038/nmeth.1514
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Impaired theta-gamma coupling in APP-deficient mice.
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- Scientific Reports, 2016, p. 21948, doi. 10.1038/srep21948
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Hippocampal Network Oscillations in APP/APLP2-Deficient Mice.
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- PLoS ONE, 2013, v. 8, n. 4, p. 1, doi. 10.1371/journal.pone.0061198
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APPsα rescues CDK5 and GSK3β dysregulation and restores normal spine density in Tau transgenic mice.
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- Frontiers in Cellular Neuroscience, 2023, v. 17, p. 1, doi. 10.3389/fncel.2023.1106176
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- Article
The Secreted β-Amyloid Precursor Protein Ectodomain APPsα Is Sufficient to Rescue the Anatomical, Behavioral, and Electrophysiological Abnormalities of APP-Deficient Mice.
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- Journal of Neuroscience, 2007, v. 27, n. 29, p. 7817, doi. 10.1523/JNEUROSCI.1026-07.2007
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Distinct in vivo roles of secreted APP ectodomain variants APPsα and APPsβ in regulation of spine density, synaptic plasticity, and cognition.
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- EMBO Journal, 2018, v. 37, n. 11, p. 1, doi. 10.15252/embj.201798335
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Amyloid precursor protein maintains constitutive and adaptive plasticity of dendritic spines in adult brain by regulating D-serine homeostasis.
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- EMBO Journal, 2016, v. 35, n. 20, p. 2213, doi. 10.15252/embj.201694085
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APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP.
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- EMBO Journal, 2011, v. 30, n. 11, p. 2266, doi. 10.1038/emboj.2011.119
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- Article
APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP.
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- EMBO Journal, 2011, v. 30, n. 11, p. 2306, doi. 10.1038/emboj.2011.164
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- Article
Choroid plexus APP regulates adult brain proliferation and animal behavior.
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- Life Science Alliance, 2021, v. 4, n. 11, p. 1, doi. 10.26508/lsa.202000703
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Consequences of Amyloid‐β Deficiency for the Liver.
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- Advanced Science, 2024, v. 11, n. 18, p. 1, doi. 10.1002/advs.202307734
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Deletion of the amyloid precursor-like protein 1 (APLP1) enhances excitatory synaptic transmission, reduces network inhibition but does not impair synaptic plasticity in the mouse dentate gyrus.
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- Journal of Comparative Neurology, 2015, v. 523, n. 11, p. 1717, doi. 10.1002/cne.23766
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Laura Adamietz, Geschlecht als Erwartung.
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- Kritische Justiz, 2012, v. 45, n. 3, p. 352
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Forum Rechtskritik: Interdisziplinäre Perspektiven.
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- Kritische Justiz, 2011, v. 44, n. 4, p. 448
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Lack of APP and APLP2 in GABAergic Forebrain Neurons Impairs Synaptic Plasticity and Cognition.
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- Cerebral Cortex, 2020, v. 30, n. 7, p. 4044, doi. 10.1093/cercor/bhaa025
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APPsα Rescues Tau-Induced Synaptic Pathology.
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- Journal of Neuroscience, 2022, v. 42, n. 29, p. 5782, doi. 10.1523/JNEUROSCI.2200-21.2022
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Amyloid-Beta Mediates Homeostatic Synaptic Plasticity.
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- Journal of Neuroscience, 2021, v. 41, n. 24, p. 5157, doi. 10.1523/JNEUROSCI.1820-20.2021
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Comparative transcriptome profiling of amyloid precursor protein family members in the adult cortex.
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- BMC Genomics, 2011, v. 12, p. 1, doi. 10.1186/1471-2164-12-160
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Comparative transcriptome profiling of amyloid precursor protein family members in the adult cortex.
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- BMC Genomics, 2011, v. 12, n. 1, p. 160, doi. 10.1186/1471-2164-12-160
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Regulatory feedback cycle of the insulin‐degrading enzyme and the amyloid precursor protein intracellular domain: Implications for Alzheimer's disease.
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- Aging Cell, 2020, v. 19, n. 11, p. 1, doi. 10.1111/acel.13264
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Upregulation of PGC-1α expression by Alzheimer's disease-associated pathway: presenilin 1/amyloid precursor protein ( APP)/intracellular domain of APP.
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- Aging Cell, 2014, v. 13, n. 2, p. 263, doi. 10.1111/acel.12183
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Contribution of GABAergic interneurons to amyloid-β plaque pathology in an APP knock-in mouse model.
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- Molecular Neurodegeneration, 2020, v. 15, n. 1, p. 1, doi. 10.1186/s13024-019-0356-y
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Amyloid Precursor Protein Protects Neuronal Network Function after Hypoxia via Control of Voltage-Gated Calcium Channels.
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- Journal of Neuroscience, 2016, v. 36, n. 32, p. 8356, doi. 10.1523/JNEUROSCI.4130-15.2016
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The APP Intracellular Domain Is Required for Normal Synaptic Morphology, Synaptic Plasticity, and Hippocampus-Dependent Behavior.
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- Journal of Neuroscience, 2015, v. 35, n. 49, p. 16018, doi. 10.1523/JNEUROSCI.2009-15.2015
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