Biology subjects

Tessitore, A.

Publications and source records attributed to Tessitore, A..

4 recordsLinked to original sources

bioRxiv2020

Brain networks and cognitive impairment in Parkinson's disease

AimThe aim of the present study is to investigate the relations between both functional connectivity and brain networks with cognitive decline, in patients with Parkinsons disease (PD). IntroductionPD phenotype is not limited to motor impairment but, rather, a wide range of non-motor disturbances can occur, cognitive impairment being one of the commonest. However, how the large-scale organization of brain activity differs in cognitively impaired patients, as opposed to cognitively preserved ones, remains poorly understood. MethodsStarting from source-reconstructed resting-state magnetoencephalography data, we applied the PLM to estimate functional connectivity, globally and between brain areas, in PD patients with and without cognitive impairment (respectively PD-CI and PD-NC), as compared to healthy subjects (HS). Furthermore, using graph analysis, we characterized the alterations in brain network topology and related these, as well as the functional connectivity, to cognitive performance. ResultsWe found reduced global and nodal PLM in several temporal (fusiform gyrus, Heschls gyrus and inferior temporal gyrus), parietal (postcentral gyrus), and occipital (lingual gyrus) areas within the left hemisphere, in the gamma band, in PD-CI patients, as compared to PD-NC and HS. With regard to the global topological features, PD-CI patients, as compared to HS and PD-NC patients, showed differences in multi frequencies bands (delta, alpha, gamma) in the Leaf fraction, Tree hierarchy (both higher in PD-CI) and Diameter (lower in PD-CI). Finally, we found statistically significant correlations between the MoCA test and both the Diameter in delta band and the Tree Hierarchy in the alpha band. ConclusionOur work points to specific large-scale rearrangements that occur selectively in cognitively compromised PD patients and correlated to cognitive impairment.

neuroscience↗

bioRxiv2019

Extensive functional repertoire underpins complex behaviours: insights from Parkinson’s disease

Rapid reconfigurations of brain activity support efficient neuronal communication and flexible behaviour. Suboptimal brain dynamics impair this adaptability, possibly leading to functional deficiencies. We hypothesize that impaired flexibility in brain activity can lead to motor and cognitive symptoms of Parkinsons disease (PD). To test this hypothesis, we studied the functional repertoire - the number of distinct configurations of neural activity - using source-reconstructed magnetoencephalography in PD patients and controls. We found stereotyped brain dynamics and reduced flexibility in PD. The intensity of this reduction was proportional to symptoms severity, which can be explained by beta-band hyper-synchronization. Moreover, the basal ganglia were prominently involved in the abnormal patterns of brain activity. Our findings support the hypotheses that: symptoms in PD reflect impaired brain flexibility, this impairment preferentially involves the basal ganglia, and beta-band hypersynchronization is associated with reduced brain flexibility. These findings highlight the importance of extensive functional repertoires for behaviour and motor.

neuroscience↗

bioRxiv2019

Effects of Post-Activation Potentiation induced by a plyometric protocol on deceleration performance.

Post-Activation Potentiation is a phenomenon by which muscular performance characteristics are acutely enhanced as a result of their previous contractile actions. It has been shown how Post-Activation Potentiation, which is usually evoked through heavy resistance exercise, has the potential to improve many different power performances, such as sprinting and jumping. Due to an easier applicability, some studies explored the potential of plyometric muscular actions to evoke the effects of Post-Activation Potentiation. Despite some findings on acceleration running performance, to the authors best knowledge, no studies investigated the effects of Post-Activation Potentiation on deceleration performance, which is a key factor in sports involving change of directions. Therefore, the aim of this study is to investigate the influence of a plyometric exercise protocol to a subsequent deceleration running performance. University soccer players (n = 18) performed 7 deceleration trials: at baseline and after [~] 15 seconds, 2, 4, 8, 12 and 16 minutes a walking control condition (C) or 3 sets of 10 repetitions of alternate-leg bounding (plyometric, P). Results show that no significant differences were found at any of the trials of the control condition (C) in comparison to the relative baseline. In the plyometric condition (P), the deceleration performance executed 2 minutes after the plyometric activity resulted significantly faster compared to the relative baseline (p = 0.042; ES = 0.86, large effect; % of improvement = 4.13 %). Therefore, the main findings of this study showed that a plyometric exercise has the potential to improve a subsequent running deceleration performance in soccer players, if an adequate recovery between these activities is provided to the players. These findings encourage further future investigations about the possible potentiating effects of plyometric activities on more complex actions like changes of direction and agility.

physiology↗

bioRxiv2018

The structural basis of lipid scrambling and inactivation in the endoplasmic reticulum scramblase TMEM16K

Membranes in cells have defined distributions of lipids in each leaflet, controlled by lipid scramblases and flip/floppases. However, for some intracellular membranes such as the endoplasmic reticulum the scramblases have not been identified. Members of the TMEM16 family have either lipid scramblase and ion channel activity, or specific chloride channel activity. Although TMEM16K is widely distributed and associated with the neurological disorder autosomal recessive spinocerebellar ataxia type 10 (SCAR10), its location in cells, function and structure are largely uncharacterised. Here we show that TMEM16K is an ER-resident calcium-regulated lipid scramblase. Our crystal structures of TMEM16K show a scramblase fold, with an open lipid transporting groove. Additional structures solved by cryo-EM reveal extensive conformational changes extending from the cytoplasmic to the ER side of the membrane, giving a state with a closed lipid permeation pathway. Molecular dynamics simulations showed that the open-groove conformation is necessary for scramblase activity. Our results suggest mechanisms by which missense variants of TMEM16K could cause SCAR10 ataxia, providing new hypotheses to explore for therapy.

biochemistry↗