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Involvement of p38 MAPK in Synaptic Function and Dysfunction

International journal of molecular sciences, 2020-08, Vol.21 (16), p.5624

2020

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Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits

Neuron (Cambridge, Mass.), 2014-09, Vol.83 (5), p.1131-1143

2014

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LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent

eLife, 2017-07, Vol.6

2017

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Mitochondrial dysfunction and mitophagy defect triggered by heterozygous GBA mutations

Autophagy, 2019-01, Vol.15 (1), p.113-130

2019

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Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach

International journal of molecular sciences, 2023-12, Vol.25 (1), p.259

2023

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Reduced gliotransmitter release from astrocytes mediates tau‐induced synaptic dysfunction in cultured hippocampal neurons

Glia, 2017-08, Vol.65 (8), p.1302-1316

2017

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Neuromodulatory Action of Picomolar Extracellular Aβ42 Oligomers on Presynaptic and Postsynaptic Mechanisms Underlying Synaptic Function and Memory

The Journal of neuroscience, 2019-07, Vol.39 (30), p.5986-6000

2019

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Synaptic Therapy in Alzheimer’s Disease: A CREB-centric Approach

Neurotherapeutics, 2015, Vol.12 (1), p.29-41

2015

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Evidence that Alzheimer's Disease Is a Disease of Competitive Synaptic Plasticity Gone Awry

Journal of Alzheimer's disease, 2024-01, Vol.99 (2), p.447-470

2024

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Genetic deletion of α7 nicotinic acetylcholine receptors induces an age-dependent Alzheimer’s disease-like pathology

Progress in neurobiology, 2021-11, Vol.206, p.102154-102154, Article 102154

2021

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Reversal of long-term dendritic spine alterations in Alzheimer disease models

Proceedings of the National Academy of Sciences - PNAS, 2009-09, Vol.106 (39), p.16877-16882

2009

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Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease

Nature Medicine, 2008-10, Vol.14 (10), p.1097-1105

2008

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Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

The Journal of clinical investigation, 2004-12, Vol.114 (11), p.1624-1634

2004

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Alzheimer's therapeutics targeting amyloid beta 1-42 oligomers II: Sigma-2/PGRMC1 receptors mediate Abeta 42 oligomer binding and synaptotoxicity

PloS one, 2014-11, Vol.9 (11), p.e111899

2014

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What Does the APP Family Do in the Brain?

Neuron (Cambridge, Mass.), 2020-11, Vol.108 (4), p.583-585

Arancio, Ottavio

2020

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Characterization and molecular profiling of PSEN1 familial Alzheimer's disease iPSC-derived neural progenitors

PloS one, 2014-01, Vol.9 (1), p.e84547-e84547

2014

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Inhibition of Histone Deacetylase 3 Restores Amyloid-β Oligomer-Induced Plasticity Deficit in Hippocampal CA1 Pyramidal Neurons

Journal of Alzheimer's disease, 2016-01, Vol.51 (3), p.783-791

2016

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Dysregulation of histone acetylation in the APP/PS1 mouse model of Alzheimer's disease

Journal of Alzheimer's disease, 2009-01, Vol.18 (1), p.131-139

2009

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FoxO1 Target Gpr17 Activates AgRP Neurons to Regulate Food Intake

Cell, 2012-06, Vol.149 (6), p.1314-1326

2012

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A time course analysis of the electrophysiological properties of neurons differentiated from human induced pluripotent stem cells (iPSCs)

PloS one, 2014-07, Vol.9 (7), p.e103418-e103418

2014

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Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

The Journal of clinical investigation, 2004-12, Vol.114 (11), p.1624-1634

2004

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Mitophagy Failure in Fibroblasts and iPSC-Derived Neurons of Alzheimer's Disease-Associated Presenilin 1 Mutation

Frontiers in molecular neuroscience, 2017-09, Vol.10, p.291-291

2017

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SARS-CoV-2 Nucleocapsid Protein Induces Tau Pathological Changes That Can Be Counteracted by SUMO2

International journal of molecular sciences, 2024-07, Vol.25 (13), p.7169

2024

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Amyloid-β Peptides Disrupt Interactions Between VAMP-2 and SNAP-25 in Neuronal Cells as Determined by FRET/FLIM

Journal of Alzheimer's disease, 2020-01, Vol.77 (1), p.423-435

2020

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Involvement of p38 MAPK in Synaptic Function and Dysfunction

Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits

LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent

Mitochondrial dysfunction and mitophagy defect triggered by heterozygous GBA mutations

Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach

Reduced gliotransmitter release from astrocytes mediates tau‐induced synaptic dysfunction in cultured hippocampal neurons

Neuromodulatory Action of Picomolar Extracellular Aβ42 Oligomers on Presynaptic and Postsynaptic Mechanisms Underlying Synaptic Function and Memory

Synaptic Therapy in Alzheimer’s Disease: A CREB-centric Approach

Evidence that Alzheimer's Disease Is a Disease of Competitive Synaptic Plasticity Gone Awry

Genetic deletion of α7 nicotinic acetylcholine receptors induces an age-dependent Alzheimer’s disease-like pathology

Reversal of long-term dendritic spine alterations in Alzheimer disease models

Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease

Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

Alzheimer's therapeutics targeting amyloid beta 1-42 oligomers II: Sigma-2/PGRMC1 receptors mediate Abeta 42 oligomer binding and synaptotoxicity

What Does the APP Family Do in the Brain?

Characterization and molecular profiling of PSEN1 familial Alzheimer's disease iPSC-derived neural progenitors

Inhibition of Histone Deacetylase 3 Restores Amyloid-β Oligomer-Induced Plasticity Deficit in Hippocampal CA1 Pyramidal Neurons

Alzheimer's therapeutics targeting amyloid beta 1-42 oligomers I: Abeta 42 oligomer binding to specific neuronal receptors is displaced by drug candidates that improve cognitive deficits

Dysregulation of histone acetylation in the APP/PS1 mouse model of Alzheimer's disease

FoxO1 Target Gpr17 Activates AgRP Neurons to Regulate Food Intake

A time course analysis of the electrophysiological properties of neurons differentiated from human induced pluripotent stem cells (iPSCs)

Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

Mitophagy Failure in Fibroblasts and iPSC-Derived Neurons of Alzheimer's Disease-Associated Presenilin 1 Mutation

SARS-CoV-2 Nucleocapsid Protein Induces Tau Pathological Changes That Can Be Counteracted by SUMO2

Amyloid-β Peptides Disrupt Interactions Between VAMP-2 and SNAP-25 in Neuronal Cells as Determined by FRET/FLIM

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