Mauro Fa’

发表

Picomolar Amyloid-β Positively Modulates Synaptic Plasticity and Memory in Hippocampus

A. Palmeri, E. Leznik, O. Arancio, 2008, The Journal of Neuroscience.

Furoxans (1,2,5-oxadiazole-N-oxides) as novel NO mimetic neuroprotective and procognitive agents.

O. Arancio, G. Thatcher, Isaac T. Schiefer, 2012, Journal of medicinal chemistry.

Design and synthesis of neuroprotective methylthiazoles and modification as NO-chimeras for neurodegenerative therapy.

O. Arancio, G. Thatcher, Jia Luo, 2012, Journal of medicinal chemistry.

Regulation of synaptic plasticity and cognition by SUMO in normal physiology and Alzheimer's disease

O. Arancio, Linda Lee, Nsikan Akpan, 2014, Scientific Reports.

α‐Synuclein involvement in hippocampal synaptic plasticity: role of NO, cGMP, cGK and CaMKII

O. Arancio, I. Ninan, Shumin Liu, 2007, The European journal of neuroscience.

Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade.

A. Palmeri, L. Honig, O. Arancio, 2018, Journal of Alzheimer's disease : JAD.

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

Miles Miller, Gary Look, Andrew F. Teich, 2014, PloS one.

Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease.

O. Arancio, S. Schmidt, P. Mathews, 2008, The Journal of clinical investigation.

Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits

O. Arancio, L. D’Adamio, R. Tamayev, 2010, Proceedings of the National Academy of Sciences.

Endogenous amyloid‐β is necessary for hippocampal synaptic plasticity and memory

A. Palmeri, O. Arancio, M. Mercken, 2011, Annals of neurology.

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

O. Arancio, D. Latchman, Hong Zhang, 2009, Journal of Alzheimer's disease : JAD.

Tau is not necessary for amyloid-beta-induced synaptic and memory impairments.

Elentina K. Argyrousi, P. Fraser, O. Arancio, 2020, The Journal of clinical investigation.

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

A. Palmeri, P. Fraser, O. Arancio, 2017, eLife.

Design, synthesis, and optimization of novel epoxide incorporating peptidomimetics as selective calpain inhibitors.

Ottavio Arancio, Pavel Petukhov, O. Arancio, 2013, Journal of medicinal chemistry.

Time-dependent reversal of synaptic plasticity induced by physiological concentrations of oligomeric Aβ42: an early index of Alzheimer’s disease

A. Palmeri, O. Arancio, I. Ninan, 2016, Scientific Reports.

Synaptic fatigue is more pronounced in the APP/PS1 transgenic mouse model of Alzheimer's disease.

Ottavio Arancio, O. Arancio, I. Ninan, 2005, Current Alzheimer research.

Dynamin 1 Is Required for Memory Formation

O. Arancio, Agnieszka Staniszewski, Yitshak I. Francis, 2014, PloS one.

Novel Selective Calpain 1 Inhibitors as Potential Therapeutics in Alzheimer's Disease.

O. Arancio, G. Thatcher, P. Petukhov, 2015, Journal of Alzheimer's disease : JAD.

Re-engineering a neuroprotective, clinical drug as a procognitive agent with high in vivo potency and with GABAA potentiating activity for use in dementia

O. Arancio, G. Thatcher, Jia Luo, 2015, BMC Neuroscience.

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

O. Arancio, Russell E Nicholls, D. Puzzo, 2015, Neurotherapeutics.

Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade

Elentina K. Argyrousi, O. Arancio, D. Puzzo, 2019, Molecular Neurodegeneration.

Preparation of oligomeric beta-amyloid 1-42 and induction of synaptic plasticity impairment on hippocampal slices.

O. Arancio, I. Orozco, Yimin Gong, 2010, Journal of visualized experiments : JoVE.

Re-engineering a neuroprotective, clinical drug as a procognitive agent with high in vivo potency and with GABAA potentiating activity for use in dementia

O. Arancio, G. Thatcher, Jia Luo, 2015, BMC Neuroscience.

Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade.

A. Palmeri, L. Honig, O. Arancio, 2019, Journal of Alzheimer's disease : JAD.

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus.

U. Hengst, C. Troy, Ying Y. Jean, 2015, Journal of visualized experiments : JoVE.

Extracellular Tau Oligomers Produce An Immediate Impairment of LTP and Memory

A. Palmeri, L. Honig, E. Sigurdsson, 2016, Scientific Reports.

O4-06-03: Amyloid-beta peptide is a positive modulator of synaptic plasticity and memory

A. Palmeri, E. Leznik, O. Arancio, 2008, Alzheimer's & Dementia.

Re-engineering a neuroprotective, clinical drug as a procognitive agent with high in vivo potency and with GABAA potentiating activity for use in dementia

O. Arancio, S. Piyankarage, L. VandeVrede, 2015, BMC Neuroscience.

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

O. Arancio, Russell E Nicholls, D. Puzzo, 2015, Neurotherapeutics.

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

Miles C. Miller, G. Rishton, O. Arancio, 2014, PloS one.

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

O. Arancio, D. Latchman, Hong Zhang, 2009, Journal of Alzheimer's disease : JAD.