Publications by authors named "E Di Florio"
Article Synopsis
- * Research indicates that the synthetic compound Trofinetide and nerve growth factor (rhNGF) may provide therapeutic benefits, as seen in both cell cultures and in vivo studies with mice lacking MECP2.
- * Positive results from treatments with rhNGF showed improved cognitive and motor abilities in both male and female mouse models of Rett syndrome, with further analysis planned to explore underlying molecular mechanisms.
Article Synopsis
- Synaptic abnormalities are a key feature in various neurological disorders, and understanding their causes is essential for developing treatments.
- Rett syndrome (RTT) is a rare disorder primarily affecting girls and is linked to mutations in a gene that impacts synaptic connectivity.
- Recent findings emphasize the role of astrocytes (supportive brain cells) in RTT, showing that those lacking a specific protein release harmful substances that disrupt synapse formation, with elevated IL-6 levels contributing to these effects.
Degeneration of dopaminergic neurons leads to Parkinson's disease (PD), characterized by reduced levels of striatal dopamine (DA) and impaired voluntary movements. DA replacement is achieved by levodopa treatment which in long-term causes involuntary movements or dyskinesia. Dyskinesia is linked to the pulsatile activation of D1 receptors of the striatal medium spiny neurons (MSNs) forming the direct output pathway (dMSNs).
View Article and Find Full Text PDFBackground And Aim Of The Work: Intramedullary nailing is a fundamental tool for the treatment of meta-diaphyseal tibia fractures. While, in the past, the infrapatellar approach was the only one available, over the last few years, an alternative approach has been developed: the suprapatellar tibial nailing. This technique has shown some advantages over the other one.
View Article and Find Full Text PDFFXYD1 is a key protein controlling ion channel transport. FXYD1 exerts its function by regulating Na/K-ATPase activity, mainly in brain and cardiac tissues. Alterations of the expression level of the FXYD1 protein cause diastolic dysfunction and arrhythmias in heart and decreased neuronal dendritic tree and spine formation in brain.
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