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Fabio Benfenati

Researcher at Istituto Italiano di Tecnologia

Publications -  424
Citations -  24243

Fabio Benfenati is an academic researcher from Istituto Italiano di Tecnologia. The author has contributed to research in topics: Synapsin & Synapsin I. The author has an hindex of 77, co-authored 406 publications receiving 21422 citations. Previous affiliations of Fabio Benfenati include University of Padua & University of Modena and Reggio Emilia.

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A hybrid bioorganic interface for neuronal photoactivation

TL;DR: It is shown that primary neurons can be successfully grown onto the polymer layer without affecting the optoelectronic properties of the active material or the biological functionality of neuronal network, and action potentials can be triggered in a temporally reliable and spatially selective manner with short pulses of visible light.
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Synapsin I Is an Oligomannose-Carrying Glycoprotein, Acts As an Oligomannose-Binding Lectin, and Promotes Neurite Outgrowth and Neuronal Survival When Released via Glia-Derived Exosomes

TL;DR: The data indicate that, under conditions of high neuronal activity and/or oxidative stress, synapsin can be released from glial-derived exosomes and promotes neurite outgrowth and neuronal survival by modulating the interactions between glia and neurons.
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The Inhibitory Effects of Interleukin‐6 on Synaptic Plasticity in the Rat Hippocampus Are Associated with an Inhibition of Mitogen‐Activated Protein Kinase ERK

TL;DR: The results indicate the tyrosine kinases and MAPK/ERK are involved in hippocampal synaptic plasticity and may represent preferential intracellular targets for the actions of IL‐6 in the adult nervous system.
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Gangliosides increase the survival of lesioned nigral dopamine neurons and favour the recovery of dopaminergic synaptic function in striatum of rats by collateral sprouting.

TL;DR: It is introduced that following ganglioside treatment some lesioned DA nerve cells do not degenerate, but elongate their dendrites to give increased trophic support to DA cell bodies with intact DA axons, and may possibly represent a new type of drug in the treatment of Parkinson's disease and aging processes in DA systems.
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Ryanodine Receptor Blockade Reduces Amyloid-β Load and Memory Impairments in Tg2576 Mouse Model of Alzheimer Disease

TL;DR: It is shown that overexpression of wild-type human APP (APP695), or APP harboring the Swedish double mutation (APPswe) triggers increased ryanodine receptor (RyR) expression and enhances RyR-mediated ER Ca2+ release in SH-SY5Y neuroblastoma cells and in APPswe-expressing (Tg2576) mice.