about
Disassembly of shank and homer synaptic clusters is driven by soluble beta-amyloid(1-40) through divergent NMDAR-dependent signalling pathwaysBotulinum toxin A treatment for primary hemifacial spasm: a 10-year multicenter study.Functional Connectivity Mapping in the Animal Model: Principles and Applications of Resting-State fMRI.From intrinsic firing properties to selective neuronal vulnerability in neurodegenerative diseases.Reversible Parkinsonian syndrome associated with anti-neuronal antibodies in acute EBV encephalitis: a case report.Down syndrome DSCR1 causes spine pathology via the Fragile X-related protein FMRP.Brain-derived neurotrophic factor and risk for primary adult-onset cranial-cervical dystonia.Amyloid-β induces caspase-dependent loss of PSD-95 and synaptophysin through NMDA receptors.Brain F-18 Fluorocholine PET/CT for the assessment of optic pathway glioma in neurofibromatosis-1.Severity of neuropsychiatric symptoms and dopamine transporter levels in dementia with Lewy bodies: a 123I-FP-CIT SPECT study.β-Site amyloid precursor protein-cleaving enzyme 1 activity is related to cerebrospinal fluid concentrations of sortilin-related receptor with A-type repeats, soluble amyloid precursor protein, and tau.Soluble beta-amyloid1-40 induces NMDA-dependent degradation of postsynaptic density-95 at glutamatergic synapses.Neddylation inhibition impairs spine development, destabilizes synapses and deteriorates cognition.Astrocytic GluN2A and GluN2B Oppose the Synaptotoxic Effects of Amyloid-β1-40 in Hippocampal Cells.Neuroprotection through excitability and mTOR required in ALS motoneurons to delay disease and extend survival.Neuroinflammation after traumatic brain injury (TBI) is enhanced in activating transcription factor 3 (ATF3) mutant mice.Hypoexcitability precedes denervation in the large fast-contracting motor units in two unrelated mouse models of ALS.Interferons in Traumatic Brain and Spinal Cord Injury: Current Evidence for Translational Application.Stage-dependent remodeling of projections to motor cortex in ALS mouse model revealed by a new variant retrograde-AAV9Interferon β-1a downregulates TNFα-induced intercellular adhesion molecule 1 expression on brain microvascular endothelial cells through a tyrosine kinase-dependent pathwayA circuit mechanism for neurodegeneration.Blepharospasm in bardet-biedl syndrome: a case reportLife-or-death decisions upon axonal damageModeling neuronal vulnerability in ALSNF-κB activation in astrocytes drives a stage-specific beneficial neuroimmunological response in ALSNutrient limitation affects presynaptic structures through dissociable Bassoon autophagic degradation and impaired vesicle releaseParvalbumin Interneurons Shape Neuronal Vulnerability in Blunt TBIA CRHR1 antagonist prevents synaptic loss and memory deficits in a trauma-induced delirium-like syndromeFocal alterations of the callosal area III in primary lateral sclerosis: An MRI planimetry and texture analysisTREM1-ors shake the brain and gut after strokeEffect of High-Caloric Nutrition on Survival in Amyotrophic Lateral SclerosisRetinoic acid worsens ATG10-dependent autophagy impairment in TBK1-mutant hiPSC-derived motoneurons through SQSTM1/p62 accumulationSTAT6 mediates the effect of ethanol on neuroinflammatory response in TBILongitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse modelSynaptic restoration by cAMP/PKA drives activity-dependent neuroprotection to motoneurons in ALSAutism-associated SHANK3 mutations impair maturation of neuromuscular junctions and striated muscles
P50
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P50
description
researcher ORCID ID = 0000-0001-9935-6899
@en
name
Francesco Roselli
@ast
Francesco Roselli
@en
Francesco Roselli
@es
Francesco Roselli
@nl
type
label
Francesco Roselli
@ast
Francesco Roselli
@en
Francesco Roselli
@es
Francesco Roselli
@nl
prefLabel
Francesco Roselli
@ast
Francesco Roselli
@en
Francesco Roselli
@es
Francesco Roselli
@nl
P21
P31
P496
0000-0001-9935-6899