Mutations in the SPAST gene causing hereditary spastic paraplegia arerelated to global topological alterations in brain functional networks

Aim: Our aim was to describe the rearrangements of the brain activity related to genetic mutations in the SPAST gene. Methods: Ten SPG4 patients and ten controls underwent a 5 min resting state magnetoencephalography recording and neurological examination. A beamformer algorithm reconstructed the activity of 90 brain areas. The phase lag index was used to estimate synchrony between brain areas. The minimum spanning tree was used to estimate topological metrics such as the leaf fraction (a measure of network integration) and the degree divergence (a measure of the resilience of the network against pathological events). The betweenness centrality (a measure to estimate the centrality of the brain areas) was used to estimate the centrality of each brain area. Results: Our results showed topological rearrangements in the beta band. Specifically, the degree divergence was lower in patients as compared to controls and this parameter related to clinical disability. No differences appeared in leaf fraction nor in betweenness centrality. Conclusion: Mutations in the SPAST gene are related to a reorganization of the brain topology

Increased Cortical Thickness in Sports Experts: A Comparison of Diving Players with the Controls

Sports experts represent a population of people who have acquired expertise in sports training and competition. Recently, the number of studies on sports experts has increased; however, neuroanatomical changes following extensive training are not fully understood. In this study, we used cortical thickness measurement to investigate the brain anatomical characteristics of professional divers with extensive training experience. A comparison of the brain anatomical characteristics of the non-athlete group with those of the athlete group revealed three regions with significantly increased cortical thickness in the athlete group. These regions included the left superior temporal sulcus, the right orbitofrontal cortex and the right parahippocampal gyrus. Moreover, a significant positive correlation between the mean cortical thickness of the right parahippocampal gyrus and the training experience was detected, which might indicate the effect of extensive training on diving players' brain structure

Effects of Speed and Extent of Stretching on the Elastic Properties of Active Frog Muscle

The work done during fast recoil of active striated muscle (as in a jump) was measured at 2 and 12 \uc2\ub0C by making tetanized frog sartorii shorten from about 2 mm above slack length, l0, at high speed(6\ue2 9 l0 s\ue2 1)(1) during a state of isometric contraction and (2) after stretching the muscle, while active, at different speeds and by different amounts. The work done increases with the force developed by the muscle according to a sigmoidal curve, having a point of inflexion that is displaced to greater values of force at 12 \uc2\ub0C than at 2 \uc2\ub0C. Previous stretching leads to an upward shift of this curve, i.e. to an iso-force gain of energy. This gain increases towards a maximum as the speed and extent of stretching are increased, attaining 60\ue2 80% of the total work done from a state of isometric contraction; this fraction decreases when stretching begins from lengths smaller than l0. The apparent elastic behaviour of muscle is thus described by a set of curves rather than by a single curve. Active muscle behaves as a more rigid structure when it transmits the generated force to an external load (as in an isometric contraction) and as a more compliant structure when, stretched by an external force, it has the opportunity to store external mechanical energy.Note

The dark sides of amyloid in Alzheimer's disease pathogenesis.

Although widely explored, the pathogenesis of Alzheimer's disease (AD) has yet to be cleared. Over the past twenty years the so call amyloid cascade hypothesis represented the main research paradigm in AD pathogenesis. In spite of its large consensus, the proposed role of β-amyloid (Aβ) remain to be elucidated. Many evidences are starting to cast doubt on Aβ as the primary causative factor in AD. For instance, Aβ is deposited in the brain following many different kinds of injury. Also, concentration of Aβ needed to induce toxicity in vitro are never reached in vivo. In this review we propose an amyloid-independent interpretation of several AD pathogenic features, such as synaptic plasticity, endo-lysosomal trafficking, cell cycle regulation and neuronal survival