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Calabresi P.,University of Perugia | Castrioto A.,University of Perugia | Castrioto A.,Joseph Fourier University | Di Filippo M.,University of Perugia | Picconi B.,Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia
The Lancet Neurology

Parkinson's disease is a common progressive neurodegenerative disease, of which the main neuropathological hallmark is dopaminergic neuronal loss. Increased attention has been directed towards non-motor symptoms in Parkinson's disease, such as cognitive impairment and behavioural disorders. Clinical and experimental findings support the view that the hippocampus, a temporal lobe structure involved in physiological learning and memory, is also implicated in the cognitive dysfunction seen in some patients with Parkinson's disease. Moreover, emerging data suggest interactions between the dopaminergic systems and the hippocampus in synaptic plasticity, adaptive memory, and motivated behaviour. This structure is also implicated in the pathophysiology of other non-motor symptoms, such as impulse control disorders, anosmia, and fatigue. Evidence from clinical observations and experimental studies suggest a complex hippocampal cross-talk among the dopaminergic and other transmitter systems. Furthermore, neurotrophic factors might interact with the hippocampal dopaminergic system having possible implications on the non-motor symptoms seen in patients with Parkinson's disease. © 2013 Elsevier Ltd. Source

Avenanti A.,University of Bologna | Avenanti A.,Centro Studi e Ricerche in Neuroscienze Cognitive | Candidi M.,Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia | Candidi M.,University of Rome La Sapienza | Urgesi C.,University of Udine
Frontiers in Human Neuroscience

Neurophysiological and imaging studies have shown that seeing the actions of other individuals brings about the vicarious activation of motor regions involved in performing the same actions. While this suggests a simulative mechanism mediating the perception of others' actions, one cannot use such evidence to make inferences about the functional significance of vicarious activations. Indeed, a central aim in social neuroscience is to comprehend how vicarious activations allow the understanding of other people's behavior, and this requires to use stimulation or lesion methods to establish causal links from brain activity to cognitive functions. In the present work we review studies investigating the effects of transient manipulations of brain activity or stable lesions in the motor system on individuals' ability to perceive and understand the actions of others. We conclude there is now compelling evidence that neural activity in the motor system is critical for such cognitive ability. More research using causal methods, however, is needed in order to disclose the limits and the conditions under which vicarious activations are required to perceive and understand actions of others as well as their emotions and somatic feelings. © 2013 Avenanti, Candidi and Urgesi. Source

Avenanti A.,Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia | Avenanti A.,University of Bologna | Avenanti A.,Centro Of Studi E Ricerche In Neuroscienze Cognitive | Sirigu A.,French National Center for Scientific Research | And 2 more authors.
Current Biology

Although social psychology studies suggest that racism often manifests itself as a lack of empathy [1, 2], i.e., the ability to share and comprehend others' feelings and intentions [3-7], evidence for differential empathic reactivity to the pain of same- or different-race individuals is meager [8, 9]. Using transcranial magnetic stimulation, we explored sensorimotor empathic brain responses [10-15] in black and white individuals who exhibited implicit but not explicit ingroup preference and race-specific autonomic reactivity [16-20]. We found that observing the pain of ingroup models inhibited the onlookers' corticospinal system as if they were feeling the pain [10-15, 21, 22]. Both black and white individuals exhibited empathic reactivity also when viewing the pain of stranger, very unfamiliar, violet-hand models. By contrast, no vicarious mapping of the pain of individuals culturally marked as outgroup members on the basis of their skin color was found. Importantly, group-specific lack of empathic reactivity was higher in the onlookers who exhibited stronger implicit racial bias. These results indicate that human beings react empathically to the pain of stranger individuals [3-7]. However, racial bias and stereotypes may change this reactivity into a group-specific lack of sensorimotor resonance [1-3, 9, 23, 24]. © 2010 Elsevier Ltd. All rights reserved. Source

Saccone V.,Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia | Consalvi S.,Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia | Giordani L.,Sanford Burnham Institute for Medical Research | Mozzetta C.,Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia | And 23 more authors.
Genes and Development

Fibro-adipogenic progenitors (FAPs) are important components of the skeletal muscle regenerative environment. Whether FAPs support muscle regeneration or promote fibro-adipogenic degeneration is emerging as a key determinant in the pathogenesis of muscular diseases, including Duchenne muscular dystrophy (DMD). However, the molecular mechanism that controls FAP lineage commitment and activity is currently unknown. We show here that an HDAC-myomiR-BAF60 variant network regulates the fate of FAPs in dystrophic muscles of mdx mice. Combinatorial analysis of gene expression microarray, genome-wide chromatin remodeling by nuclease accessibility (NA) combined with next-generation sequencing (NA-seq), small RNA sequencing (RNA-seq), and microRNA (miR) high-throughput screening (HTS) against SWI/SNF BAF60 variants revealed that HDAC inhibitors (HDACis) derepress a "latent" myogenic program in FAPs from dystrophic muscles at early stages of disease. Specifically, HDAC inhibition induces two core components of the myogenic transcriptional machinery, MYOD and BAF60C, and up-regulates the myogenic miRs (myomiRs) (miR-1.2, miR-133, and miR-206), which target the alternative BAF60 variants BAF60A and BAF60B, ultimately directing promyogenic differentiation while suppressing the fibro-adipogenic phenotype. In contrast, FAPs from late stage dystrophic muscles are resistant to HDACi-induced chromatin remodeling at myogenic loci and fail to activate the promyogenic phenotype. These results reveal a previously unappreciated disease stage-specific bipotency of mesenchimal cells within the regenerative environment of dystrophic muscles. Resolution of such bipotency by epigenetic intervention with HDACis provides a molecular rationale for the in situ reprogramming of target cells to promote therapeutic regeneration of dystrophic muscles. © 2014 Saccone et al. Source

Gravina P.,Clinical Molecular Biology Laboratory | Gravina P.,University of Rome Tor Vergata | Spoletini I.,Istituto di Ricovero e Cura a Carattere Scientifico Fondazione Santa Lucia | Masini S.,University of Rome Tor Vergata | And 9 more authors.
Psychiatry Research

Oxidative damage is thought to play a role in the predisposition to schizophrenia. We determined if the polymorphisms of the GSTP1, GSTM1, GSTT1 and GSTA1 genes, which affect the activity of these enzymes against oxidative stress, have a role as susceptibility genes for schizophrenia, analyzing 138 schizophrenic patients and 133 healthy controls. We found that the combination of the absence of GSTM1 gene with the of the GSTM1 gene with the polymorphism GSTA1*B/*B, and the presence of the GSTT1 gene, represents a risk factor for schizophrenia, indicating that the combination of different GST polymorphisms has a role in the predisposition to schizophrenia, probably affecting the capacity of the cell to detoxify the oxidized metabolites of catecholamines. © 2010 Elsevier Ireland Ltd. Source

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