Francesca Biagioni

ORCID: 0000-0003-3566-4889
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About
Contact & Profiles
Research Areas
  • Parkinson's Disease Mechanisms and Treatments
  • Neuroscience and Neuropharmacology Research
  • Autophagy in Disease and Therapy
  • Alzheimer's disease research and treatments
  • Neurological disorders and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Amyotrophic Lateral Sclerosis Research
  • Neurotransmitter Receptor Influence on Behavior
  • Cannabis and Cannabinoid Research
  • Prion Diseases and Protein Misfolding
  • Neurological diseases and metabolism
  • Neurogenetic and Muscular Disorders Research
  • MicroRNA in disease regulation
  • Nuclear Receptors and Signaling
  • Genetic Neurodegenerative Diseases
  • Nerve injury and regeneration
  • Epilepsy research and treatment
  • Circular RNAs in diseases
  • Neurogenesis and neuroplasticity mechanisms
  • Retinal Diseases and Treatments
  • RNA regulation and disease
  • Biomarkers in Disease Mechanisms
  • Cancer-related molecular mechanisms research
  • Endoplasmic Reticulum Stress and Disease
  • Mitochondrial Function and Pathology

Istituto Neurologico Mediterraneo
2016-2025

Istituti di Ricovero e Cura a Carattere Scientifico
2016-2024

University of Salerno
2015

Morpho (United States)
2015

University of Pisa
2006-2015

University of Naples Federico II
2015

National Research Council
2015

Parco Tecnologico Padano
2012

University of Brescia
2005

Pentraxin 3 (PTX3), the prototype of long pentraxins, has been described to be associated with endothelial dysfunction in different cardiovascular disorders. No study yet evaluated possible direct effect PTX3 on vascular function.Through vitro experiments reactivity and ultrastructural analyses, we demonstrate that induces morphological changes layer through a P-selectin/matrix metalloproteinase-1 pathway. The latter hampered detachment nitric oxide synthase from caveolin-1, leading an...

10.1161/circulationaha.114.014822 article EN Circulation 2015-03-07

Expression of Dickkopf-1 (Dkk-1), a secreted protein that negatively modulates the Wnt pathway, was induced in hippocampus gerbils and rats subjected to transient global cerebral ischemia as well cultured cortical neurons challenged with an excitotoxic pulse. In ischemic animals, temporal regional pattern Dkk-1 expression correlated profile neuronal death, assessed by Nissl staining immunostaining adjacent hippocampal sections. Treatment animals either antisense oligonucleotides or lithium...

10.1523/jneurosci.5230-04.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-03-09

We examined whether selective activation of mGlu4 metabotropic glutamate receptors attenuates 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigrostriatal damage in mice. C57BL mice were treated with a single dose MPTP (30 mg/kg, i.p.) preceded, 30 min earlier, by systemic injection the receptor enhancer N -phenyl-7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxamide (PHCCC). PHCCC was injected either subcutaneously cremophor EL or intraperitoneally saline containing 50% DMSO....

10.1523/jneurosci.1595-06.2006 article EN cc-by-nc-sa Journal of Neuroscience 2006-07-05

Inhibition of the canonical Wnt pathway has been implicated in pathophysiology neuronal death. Here, we report that secreted antagonist, Dickkopf-1 (Dkk-1) is rapidly induced neurons after induction focal brain ischemia. In rats undergoing transient ischemia response to infusion endothelin-1, Dkk-1 was ischemic core and penumbra region. Induction associated with a reduced expression beta-catenin (a downstream signaling molecule pathway), not observed expressing protective protein, heat shock...

10.1038/jcbfm.2008.111 article EN Journal of Cerebral Blood Flow & Metabolism 2008-10-01

Amphetamine (AMPH) and methamphetamine (METH) are widely abused psychostimulants, which produce a variety of psychomotor, autonomic neurotoxic effects. The behavioral effects both compounds (from now on defined as AMPHs) stem from fair molecular anatomical specificity for catecholamine-containing neurons, placed in the brainstem reticular formation. In fact, structural cross-affinity joined with presence shared targets between AMPHs catecholamine provides basis quite selective recruitment...

10.3389/fnana.2019.00048 article EN cc-by Frontiers in Neuroanatomy 2019-05-10

We combined the use of knock-out mice and subtype-selective antagonists [2-methyl-6-(phenylethynyl)pyridine (MPEP) (E)-2-methyl-6-(2-phenylethenyl)-pyridine (SIB1893)] to examine whether endogenous activation mGlu5 metabotropic glutamate receptors contributes pathophysiology nigro-striatal damage in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model parkinsonism. High doses MPTP (four injections 20 mg/kg, i.p., every 2 hr) induced a high mortality rate nearly total degeneration...

10.1523/jneurosci.3831-03.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-01-28

Summary: Inhibition of the Wnt pathway by secreted glycoprotein, Dickkopf‐1 (Dkk‐1) has been related to processes excitotoxic and ischemic neuronal death. We now report that Dkk‐1 is induced in neurons rat olfactory cortex hippocampus degenerating response seizures produced systemic injection kainate (12 mg/kg, i.p.). There was a tight correlation between expression death both regions, as shown different profiles animals classified “high” “low” responders kainate. For example, no induction...

10.1111/j.1528-1167.2007.01055.x article EN Epilepsia 2007-03-13

Abstract Background Spinocerebellar ataxia type 1 (SCA1) is a genetic disorder characterized by severe associated with progressive loss of cerebellar Purkinje cells. The mGlu1 metabotropic glutamate receptor plays key role in mechanisms activity-dependent synaptic plasticity the cerebellum, and its dysfunction linked to pathophysiology motor symptoms SCA1. We used SCA1 heterozygous transgenic mice (Q154/Q2) as model for testing hypothesis that drugs enhance function may be good candidates...

10.1186/1756-6606-6-48 article EN cc-by Molecular Brain 2013-11-19
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