A5083504536- Neurological disorders and treatments
- Parkinson's Disease Mechanisms and Treatments
- Neuroscience and Neuropharmacology Research
- Nuclear Receptors and Signaling
- Neurotransmitter Receptor Influence on Behavior
- Neuroinflammation and Neurodegeneration Mechanisms
- Genetic Neurodegenerative Diseases
- Neuroendocrine regulation and behavior
- Memory and Neural Mechanisms
- Adenosine and Purinergic Signaling
- Transcranial Magnetic Stimulation Studies
- Neural dynamics and brain function
- Trace Elements in Health
- EEG and Brain-Computer Interfaces
- Dialysis and Renal Disease Management
- Muscle metabolism and nutrition
- Neuroscience and Neural Engineering
- Diet and metabolism studies
- Nutrition and Health in Aging
- Neurogenesis and neuroplasticity mechanisms
- Tryptophan and brain disorders
- Sleep and Wakefulness Research
- Neurological and metabolic disorders
- Drug Transport and Resistance Mechanisms
- Muscle Physiology and Disorders
Università Cattolica del Sacro Cuore
2021-2025
University of Geneva
2022
University of Perugia
2019-2021
Fondazione Santa Lucia
2018-2021
Istituti di Ricovero e Cura a Carattere Scientifico
2019-2020
Optimisation Thérapeutique en Neuropsychopharmacologie
2020
Université Paris Cité
2020
Inserm
2020
Neuroinflammation is one of the hallmarks Parkinson's disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, effects stimulating resolution in PD - modulate progression still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA properties, reduced...
Parkinson's disease is a progressive neurodegenerative disorder characterized by altered striatal dopaminergic signalling that leads to motor and cognitive deficits. also abnormal presence of soluble toxic forms α-synuclein that, when clustered into Lewy bodies, represents one the pathological hallmarks disease. However, oligomers might directly affect synaptic transmission plasticity in models. Accordingly, combining electrophysiological, optogenetic, immunofluorescence, molecular...
Intensive physical activity improves motor functions in patients with Parkinson's disease (PD) at early stages. However, the mechanisms underlying beneficial effects of exercise on PD-associated neuronal alterations have not been fully clarified yet. Here, we tested hypothesis that an intensive treadmill training program rescues striatal plasticity and cognitive deficits rats receiving intrastriatal injection alpha-synuclein (α-syn) preformed fibrils. Improved control visuospatial learning...
Since both serotonergic and dopaminergic afferents densely innervate many parts of the central nervous system, intact crosstalk between serotonin (5-HT) dopamine (DA) transmission is essential for regulating synaptic plasticity in striatum (STR), prefrontal cortex (PFC), hippocampus (HPC).. Experimental models have provided strong evidence a synergistic action DA 5-HT convergent release PFC, HPC, STR to modulate motor control, learning, memory processes. In this review, we will discuss...
Organic cation transporters (OCTs) participate in the handling of compounds kidneys and at synaptic cleft. Their role blood-brain barrier (BBB) brain drug delivery is still unclear. The presence OCT1,2,3 (SLC22A1-3) mouse, rat human isolated microvessels was investigated by either qRT-PCR, quantitative proteomics and/or functional studies. BBB transport prototypical substrate [3H]-1-methyl-4-phenylpyridinium ([3H]-MPP+) measured situ perfusion six mouse strains Sprague Dawley rats, primary...
Levodopa (L-DOPA) treatment is the main gold-standard therapy for Parkinson's disease (PD). Besides good antiparkinsonian effects, prolonged use of this drug associated to development involuntary movements known as L-DOPA-induced dyskinesia (LID). LID linked a sensitization dopamine (DA) D1 receptors located on spiny projection neurons (SPNs) dorsal striatum. Several evidences have shown that emergence can be related striatal D1/cAMP/PKA/DARPP-32 and extracellular signal-regulated kinases...
Abstract Background In experimental models of Parkinson's disease (PD), different degrees degeneration to the nigrostriatal pathway produce distinct profiles synaptic alterations that depend on progressive changes in N‐methyl‐D‐aspartate receptors (NMDAR)‐mediated functions. Repetitive transcranial magnetic stimulation (rTMS) induces modifications glutamatergic and dopaminergic systems, suggesting it may have an impact synapses modulated by dopamine neurotransmission. However, no studies so...
Patients affected by chronic kidney disease (CKD) have an increased risk of developing cognitive impairment. The cause mental health disorders in CKD and hemodialysis patients is multifactorial, due to the interaction classical cardiovascular factors, kidney- dialysis-related factors with depression, multiple drugs overuse. A large number compounds, defined as uremic toxins that normally are excreted healthy kidneys, accumulate circulations, tissues, organs patients. Among candidate several...
Treatment with L-3,4-dihydroxyphenylalanine (L-Dopa) compensates for decreased striatal dopamine (DA) levels and reduces Parkinson's disease (PD) symptoms. However, during progression, L-Dopa-induced dyskinesia (LID) develops virtually in all PD patients, making the control of symptoms difficult. Thus, understanding mechanisms underlying LID these motor abnormalities is a major issue care patients. From experimental clinical studies, complex cascade molecular cellular events emerges, but...
Abstract Background Prolonged dopaminergic replacement therapy in PD results pulsatile dopamine receptors stimulation both dorsal and ventral striatum causing wearing off, motor fluctuations, nonmotor side effects such as behavioral addictions. Among impulse control disorders, binge eating can be easily modeled laboratory animals. Objectives We hypothesize that manipulation of levels a 6‐hydroxydopamine–lesioned rats, model characterized by different extent denervation between striatum,...
Abstract Huntington's disease (HD) is a genetic neurodegenerative condition characterized by abnormal dopamine (DA)–glutamate interactions, severe alterations in motor control, and reduced behavioral flexibility. Experimental models of show that during symptomatic phases, HD shares with other hyperkinetic disorders the loss synaptic depotentiation striatal spiny projection neurons (SPNs). Here we test hypothesis corticostriatal long‐term depression (LTD), well‐conserved scaling down response...
Plasticity at corticostriatal synapses is a key substrate for variety of brain functions – including motor control, learning and reward processing often disrupted in disease conditions. Despite intense research pointing toward dynamic interplay between glutamate, dopamine (DA), serotonin (5-HT) neurotransmission, their precise circuit synaptic mechanisms regulating role striatal plasticity are still unclear. Here, we analyze the serotonergic raphe-striatal innervation regulation DA-dependent...
Food restriction is a robust nongenic, nonsurgical and nonpharmacologic intervention known to improve health extend lifespan in various species. considered the most essential frequently consumed natural reward, current observations have demonstrated homeostatic responses neuroadaptations sustained intermittent or chronic deprivation. Results obtained date indicate that food deprivation affects glutamatergic synapses, favoring insertion of GluA2-lacking...
Abstract The decision to approach or avoid a conspecific is fundamental for survival. Affiliative (prosocial) interactions favor behaviors, while antagonistic (aggressive) contacts trigger avoidance. Here we ask how the brain encodes valence of social interaction. We focused on nucleus accumbens (NAc), region implicated in reward processing. observed that activate D1-expressing medium spiny neurons (D1-MSNs) regardless their valence. However, afferent anterior insular cortex (AIC) exhibited...
Abstract The decision to approach or avoid a conspecific is fundamental for survival. Affiliative (prosocial) interactions favor behaviors, while antagonistic (aggressive) contacts trigger avoidance. Here we ask how the brain encodes valence of social interaction. We focused on nucleus accumbens (NAc), region implicated in reward processing. observed that activate D1-expressing medium spiny neurons (D1-MSNs) regardless their valence. However, afferent D1- expressing anterior insular cortex...