A5055817499- Neuroscience and Neuropharmacology Research
- Parkinson's Disease Mechanisms and Treatments
- Nerve injury and regeneration
- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Prion Diseases and Protein Misfolding
- Signaling Pathways in Disease
- Neurotransmitter Receptor Influence on Behavior
- Cannabis and Cannabinoid Research
- Trace Elements in Health
- Neurological disorders and treatments
- Nuclear Receptors and Signaling
- Neuroscience and Neural Engineering
- Amino Acid Enzymes and Metabolism
- Neonatal and fetal brain pathology
- Botulinum Toxin and Related Neurological Disorders
- Epilepsy research and treatment
- Infectious Encephalopathies and Encephalitis
- Lipid metabolism and disorders
- Pluripotent Stem Cells Research
- Neurological diseases and metabolism
- RNA regulation and disease
- Bacterial Infections and Vaccines
- Drug Transport and Resistance Mechanisms
- Tryptophan and brain disorders
Mario Negri Institute for Pharmacological Research
2015-2025
Istituti di Ricovero e Cura a Carattere Scientifico
2014-2024
Cardiff University
2009-2016
Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele
2014
Sapienza University of Rome
2006
l -dopa–induced dyskinesia (LID) is a common debilitating complication of dopamine replacement therapy in Parkinson's disease. Recent evidence suggests that LID may be linked causally to hyperactivation the Ras–ERK signaling cascade basal ganglia. We set out determine whether specific targeting Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1), brain-specific activator pathway, provide for LID. On rodent abnormal involuntary movements scale, Ras-GRF1–deficient mice were significantly...
Parkinson's disease and related disorders are devastating neurodegenerative pathologies. Since α-synuclein was identified as a main component of Lewy bodies neurites, efforts have been made to clarify the pathogenic mechanisms α-synuclein's detrimental effects. oligomers most harmful species may recruit activate glial cells. Inflammation is emerging bridge between genetic susceptibility environmental factors co-fostering disease. However, direct evidence linking inflammation activities or...
Abstract Objective Microgliosis occurs in animal models of acquired epilepsy and patients. It includes cell proliferation that is associated with seizure frequency decreased neuronal cells human epilepsy. The role microglia the development unknown; thus, we examined its contribution to spontaneous seizure, neurodegeneration, cognitive deficits different disease phases. Methods We used a model triggered by intra‐amygdala kainic acid C57BL6N adult male mice. Mice were...
Abstract Aims The causes of distinct patterns reduced cortical thickness in the common human epilepsies, detectable on neuroimaging and with important clinical consequences, are unknown. We investigated underlying mechanisms thinning using a systems‐level analysis. Methods Imaging‐based structural maps from large‐scale epilepsy study were overlaid highly spatially resolved brain gene expression data Allen Human Brain Atlas. Cell‐type deconvolution, differential analysis cell‐type enrichment...
Highlights d eCBs govern LTD in striatopallidal neurons and adenosine does so striatonigral cells Parkinson's disease (PD)-like dopamine (DA) depletion impairs eCB-
Brain ischemia is a common acute injury resulting from impaired blood flow to the brain. Translation of effective drug candidates experimental models patients has systematically failed. The use human induced pluripotent stem cells (iPSC) offers new opportunities gain translational insights into diseases including brain ischemia. We used 3D self-assembling iPSC-derived model (human cortical organoids, hCO) characterize effects caused by oxygen-glucose deprivation (OGD). hCO exposed 2 h or 8...
Deposition of abnormally phosphorylated tau aggregates is a central event leading to neuronal dysfunction and death in Alzheimer's disease (AD) other tauopathies. Among aggregates, oligomers (TauOs) are considered the most toxic. AD brains show significant increase TauOs compared healthy controls, their concentration correlating with severity cognitive deficits progression. In vitro vivo TauO exposure leads synaptic dysfunction, but mechanisms action unclear. Evidence suggests that cellular...
Abstract Prion diseases are rare neurodegenerative conditions associated with the conformational conversion of cellular prion protein (PrP C ) into PrP Sc , a self-replicating isoform (prion) that accumulates in central nervous system affected individuals. The structure is poorly defined and likely to be heterogeneous, as suggested by existence different strains. latter represents relevant problem for therapy diseases, some potent anti-prion compounds have shown strain-specificity. Designing...
Abstract Aggregation and cytoplasmic mislocalization of TDP-43 are pathological hallmarks amyotrophic lateral sclerosis frontotemporal dementia spectrum. However, the molecular mechanism by which aggregates form cause neurodegeneration remains poorly understood. Cyclophilin A, also known as peptidyl-prolyl cis-trans isomerase A (PPIA), is a foldase chaperone. We previously found that PPIA interacts with governs some its functions, deficiency accelerates disease in mouse model sclerosis. Here...
FIRES is a rare epileptic encephalopathy induced by acute unremitting seizures that occur suddenly in healthy children or young adults after febrile illness the preceding 2 weeks. This condition results high mortality, neurological disability, and drug-resistant epilepsy. The development of new therapeutics hampered lack validated experimental models. Our goal was to address this unmet need providing simple tool for rapid throughput screening therapies target pathological inflammatory...
Chronic exposure to Δ9-tetrahydrocannabinol (THC) induces tolerance cannabinoid-induced locomotor effects, which are mediated by cannabinoid receptors (CB1Rs) located in motor control regions, including the cerebellum. There is substantial evidence of cerebellar CB1R molecular adaptation and modifications receptor signaling after prolonged exposure. However, very little known about effects chronic administration on synaptic plasticity, may contribute development behavioral tolerance. In...
Some mutant forms of the cellular prion protein (PrPC) carrying artificial deletions or point mutations associated with familial human diseases are capable inducing spontaneous ionic currents across cell membrane, conferring hypersensitivity to certain antibiotics a wide range cultured cells and primary cerebellar granular neurons (CGNs). These effects abrogated when wild type (WT) form is co-expressed, suggesting that they might be related physiological activity PrPC. Interestingly, family...
Abstract Background The role of oligomeric forms various proteins as direct responsible neuronal dysfunction in neurodegenerative disorders has been supported by numerous findings at experimental level and, more recently, histological examinations human material. cellular prion protein (PrP C ) proposed to mediate the neurotoxicity β‐amyloid, α‐synuclein and tau oligomers. We demonstrated that although amyloid‐β oligomers (AβOs) bind with high affinity PrP , memory deficit induced...