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Rosa Luisa Potenza

Researcher at Istituto Superiore di Sanità

Publications -  38
Citations -  1350

Rosa Luisa Potenza is an academic researcher from Istituto Superiore di Sanità. The author has contributed to research in topics: Adenosine A2A receptor & Receptor. The author has an hindex of 22, co-authored 36 publications receiving 1237 citations. Previous affiliations of Rosa Luisa Potenza include Sapienza University of Rome.

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Nonmotor symptoms in Parkinson's disease: investigating early-phase onset of behavioral dysfunction in the 6-hydroxydopamine-lesioned rat model.

TL;DR: Overall, the PD rat model used here displays behavioral alterations having face validity with psychiatric symptoms of the pathology and thus appears to be a valuable tool for investigating the neural bases of the early phases of PD.
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Adenosine A(2A) receptors are required for normal BDNF levels and BDNF-induced potentiation of synaptic transmission in the mouse hippocampus.

TL;DR: Results indicate that the tonic activation of A2ARs is required for BDNF‐induced potentiation of synaptic transmission and for sustaining a normal BDNF tone in the hippocampus.
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Spinal cord pathology is ameliorated by P2X7 antagonism in a SOD1-mutant mouse model of amyotrophic lateral sclerosis.

TL;DR: The antagonist Brilliant Blue G (BBG), a blood-brain barrier permeable and safe drug that has already been proven to reduce neuroinflammation in traumatic brain injury, cerebral ischemia-reperfusion, neuropathic pain and experimental autoimmune encephalitis, is used to prove the twofold role of P2X7 in the course of ALS and establish that P2x7 modulation might represent a promising therapeutic strategy by interfering with the neuroinflammatory component of the disease.
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Modulation of glutamate release and excitotoxicity by adenosine A2A receptors.

TL;DR: In conclusion, A2A antagonists show clear neuroprotective effects in models of brain injury, although their actual therapeutic potential needs to be confirmed in a wider range of doses and in Models of neurodegenerative diseases in which presynaptic and postsynaptic effects play different relative roles.