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Renata Bartesaghi

Researcher at University of Bologna

Publications -  99
Citations -  3873

Renata Bartesaghi is an academic researcher from University of Bologna. The author has contributed to research in topics: Dentate gyrus & Neurogenesis. The author has an hindex of 33, co-authored 96 publications receiving 3343 citations.

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Changes in hippocampal morphology and neuroplasticity induced by adolescent THC treatment are associated with cognitive impairment in adulthood.

TL;DR: The data suggest that THC pretreated rats may establish less synaptic contacts and/or less efficient synaptic connections throughout the hippocampus and this could represent the molecular underpinning of the cognitive deficit induced by adolescent THC treatment.
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Neurogenesis impairment and increased cell death reduce total neuron number in the hippocampal region of fetuses with Down syndrome.

TL;DR: In this paper, the authors found evidence for reduced cell proliferation in the dentate gyrus (DG) of fetuses with Down syndrome (DS), suggesting that the hippocampal hypoplasia seen in adulthood may be caused by defective early neuron production.
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Cell cycle alteration and decreased cell proliferation in the hippocampal dentate gyrus and in the neocortical germinal matrix of fetuses with Down syndrome and in Ts65Dn mice.

TL;DR: Comparisons for impaired neurogenesis in the hippocampal dentate gyrus of DS fetuses and Ts65Dn mice are obtained, providing novel evidence for proliferation impairment and suggesting that cell cycle alterations may be critical determinants of the reduced proliferation potency.
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Early Pharmacotherapy Restores Neurogenesis and Cognitive Performance in the Ts65Dn Mouse Model for Down Syndrome

TL;DR: Results show that early pharmacotherapy with a drug usable by humans can correct neurogenesis and behavioral impairment in a model for DS, and that proliferation was completely rescued by fluoxetine.
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Nitric oxide regulates cGMP-dependent cAMP-responsive element binding protein phosphorylation and Bcl-2 expression in cerebellar neurons: implication for a survival role of nitric oxide.

TL;DR: The role of CREB is confirmed in neuronal survival by demonstrating that blocking its production down‐regulates the activity of cAMP‐responsive element binding protein (CREB), a transcription factor involved in cell survival and synaptic plasticity and circumstantial evidence for a novel link among NO, CREB activation and survival is provided.