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Binetti N.,Fondazione Santa Lucia IRCCS
Journal of vision | Year: 2012

Several studies show that visual stimuli traveling at higher velocities are overestimated with respect to slower, or stationary, stimuli of equivalent physical duration. This effect-time dilation-relates more in general to several accounts highlighting a quantitative relationship between the amount of changes a stimulus is subject to and the perceived duration: faster stimuli, subject to a greater number of changes in space, lead to overestimated durations of displacement. In the present paper we provide evidence of a new illusory effect, in which the apparent duration of a sensory event is affected by the way a constant number of changes are delivered in time, or in time and space. Participants judged accelerating and decelerating sequences of stationary flickering stimuli (Experiments 1 and 3) and accelerating and decelerating horizontally drifting visual stimuli (Experiment 2) on the fronto-parallel plane. Acceleration and deceleration were achieved by irregular sequencing of events in time (anisochronous flicker rate) or irregular sequencing of events in time and space (anisochronous and/or anisometric drift). Despite being characterized by the same amounts of visual changes, accelerating and decelerating sequences lead to opposite duration biases (underestimation and overestimation errors, respectively). We refer to this effect in terms of ATI: Aniso-Time-Illusion. This bias was observed in both subsecond (760 ms) and suprasecond ranges (1900 ms). These data highlight how the spatio-temporal evolution of dynamic visual events, asides the overall quantity of changes they are subject to, affect the perceived amount of time they require to unfold.

Achsel T.,Catholic University of Leuven | Barabino S.,University of Milan Bicocca | Cozzolino M.,CNR Institute of Neuroscience | Carr M.T.,Fondazione Santa Lucia IRCCS | Carr M.T.,University of Rome Tor Vergata
Biochemical Society Transactions | Year: 2013

MNDs (motor neuron diseases) form a heterogeneous group of pathologies characterized by the progressivedegeneration of motor neurons. More and more genetic factors associated with MND encode proteinsthat have a function in RNA metabolism, suggesting that disturbed RNA metabolism could be a commonunderlying problem in several, perhaps all, forms of MND. In the present paper we review recentdevelopments showing a functional link between SMN (survival of motor neuron), the causative factorof SMA (spinal muscular atrophy), and FUS (fused in sarcoma), a genetic factor in ALS (amyotrophic lateralsclerosis). SMN is long known to have a crucial role in the biogenesis and localization of the spliceosomalsnRNPs (small nuclear ribonucleoproteins), which are essential assembly modules of the splicing machinery.Now we know that FUS interacts with SMN and pathogenic FUS mutations have a significant effect on snRNPlocalization. Together with other recently published evidence, this finding potentially links ALS pathogenesisto disturbances in the splicing machinery, and implies that pre-mRNA splicing may be the common weakpoint in MND, although other steps in mRNA metabolism could also play a role. Certainly, further comparisonof the RNA metabolism in different MND will greatly help our understanding of the molecular causes ofthese devastating diseases. © 2013 Biochemical Society.

Dinuzzo M.,University of Rome La Sapienza | Mangia S.,University of Minnesota | Maraviglia B.,University of Rome La Sapienza | Giove F.,Fondazione Santa Lucia IRCCS | Giove F.,Museo Storico Della Fisica E Centro Of Studi E Ricerche Enrico Fermi
Journal of Cerebral Blood Flow and Metabolism | Year: 2010

In this paper, we combined several mathematical models of cerebral metabolism and nutrient transport to investigate the energetic significance of metabolite trafficking within the brain parenchyma during a 360-secs activation. Glycolytic and oxidative cellular metabolism were homogeneously modeled between neurons and astrocytes, and the stimulation-induced neuronal versus astrocytic Na inflow was set to 3:1. These assumptions resemble physiologic conditions and are supported by current literature. Simulations showed that glucose diffusion to the interstitium through basal lamina dominates the provision of the sugar to both neurons and astrocytes, whereas astrocytic endfeet transfer less than 4% of the total glucose supplied to the tissue. Neuronal access to paracellularly diffused glucose prevails even after halving (doubling) the ratio of neuronal versus astrocytic glycolytic (oxidative) metabolism, as well as after reducing the neuronal versus astrocytic Na+ inflow to a nonphysiologic value of 1:1. Noticeably, displaced glucose equivalents as intercellularly shuttled lactate account for ∼ 6% to 7% of total brain glucose uptake, an amount comparable with the concomitant drainage of the monocarboxylate by the bloodstream. Overall, our results suggest that the control of carbon recruitment for neurons and astrocytes is exerted at the level of glucose uptake rather than that of lactate shuttle. © 2010 ISCBFM All rights reserved.

Kohler S.,Maastricht University | Buntinx F.,Maastricht University | Buntinx F.,Catholic University of Leuven | Palmer K.,Fondazione Santa Lucia IRCCS | Van Den Akker M.,Maastricht University
Journal of the American Geriatrics Society | Year: 2015

Objectives To study the interaction between and timing effects of depression and vascular disorders on dementia risk. Design Retrospective cohort study. Setting Primary care practices in the south of the Netherlands. Participants Individuals in primary care aged 50 to 100 followed for 13 years (N = 35,791). Measurements Medical diagnoses of incident depression, hypertension, obesity, type 2 diabetes mellitus, stroke, and dementia were extracted from a research database. Cox proportional hazards regression was used to test whether incident depression predicted dementia and its putative interactions with vascular factors. Results In total, 1,680 participants developed dementia. Individuals with depression (n = 978) had a higher risk of dementia (adjusted hazard ratio (HR) = 2.03, 95% confidence interval (CI) = 1.56-2.64). Depression exerted most effect in participants with incident stroke (HR = 5.29, 95% CI = 2.52-11.14) or newly diagnosed hypertension (HR = 3.09, 95% CI = 1.54-6.20). Conclusion Depression in later life increases the risk of dementia. The effect is particularly high in individuals with depression and vascular disorders. Targeting late-onset depression in individuals with vascular disorders might lower dementia risk by preventing cerebrovascular changes. © 2015, Copyright the Authors Journal compilation © 2015, The American Geriatrics Society.

Crosio C.,University of Sassari | Valle C.,Fondazione Santa Lucia IRCCS | Valle C.,National Research Council Italy | Casciati A.,Fondazione Santa Lucia IRCCS | And 3 more authors.
PLoS ONE | Year: 2011

Motor neuron death in amyotrophic lateral sclerosis (ALS) is considered a "non-cell autonomous" process, with astrocytes playing a critical role in disease progression. Glial cells are activated early in transgenic mice expressing mutant SOD1, suggesting that neuroinflammation has a relevant role in the cascade of events that trigger the death of motor neurons. An inflammatory cascade including COX2 expression, secretion of cytokines and release of NO from astrocytes may descend from activation of a NF-κB-mediated pathway observed in astrocytes from ALS patients and in experimental models. We have attempted rescue of transgenic mutant SOD1 mice through the inhibition of the NF-κB pathway selectively in astrocytes. Here we show that despite efficient inhibition of this major pathway, double transgenic mice expressing the mutant SOD1G93A ubiquitously and the dominant negative form of IκBα (IκBαAA) in astrocytes under control of the GFAP promoter show no benefit in terms of onset and progression of disease. Our data indicate that motor neuron death in ALS cannot be prevented by inhibition of a single inflammatory pathway because alternative pathways are activated in the presence of a persistent toxic stimulus. © 2011 Crosio et al.

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