Much evidence shows that physical exercise (PE) is a strong gene modulator that induces structural and functional changes in the brain, determining enormous benefit on both cognitive functioning and wellbeing. PE is also a protective factor for neurodegeneration. However, it is unclear if such protection is granted through modifications to the biological mechanisms underlying neurodegeneration or through better compensation against attacks. This concise review addresses the biological and psychological positive effects of PE describing the results obtained on brain plasticity and epigenetic mechanisms in animal and human studies, in order to clarify how to maximize the positive effects of PE while avoiding negative consequences, as in the case of exercise addiction.

BackgroundHuntington's disease (HD) is a fatal inherited neurodegenerative disease, caused by a

In recent years, the meaning of successful living has moved from extending lifetime to improving the quality of aging, mainly in terms of high cognitive and physical functioning together with avoiding diseases. In healthy elderly, falls represent an alarming accident both in terms of number of events and the consequent decrease in the quality of life. Stability control is a key approach for studying the genesis of falls, for detecting the event and trying to develop methodologies to prevent it. Wearable sensors have proved to be very useful in monitoring and analyzing the stability of subjects. Within this manuscript, a review of the approaches proposed in the literature for fall risk assessment, fall prevention and fall detection in healthy elderly is provided. The review has been carried out by using the most adopted publication databases and by defining a search strategy based on keywords and boolean algebra constructs. The analysis aims at evaluating the state of the art of such kind of monitoring, both in terms of most adopted sensor technologies and of their location on the human body. The review has been extended to both dynamic and static analyses. In order to provide a useful tool for researchers involved in this field, the manuscript also focuses on the tests conducted in the analyzed studies, mainly in terms of characteristics of the population involved and of the tasks used. Finally, the main trends related to sensor typology, sensor location and tasks have been identified.

BackgroundFriedreich's ataxia (FRDA) is the most common hereditary ataxia among caucasians. The molecular defect in FRDA is the trinucleotide GAA expansion in the first intron of the FXN gene, which encodes frataxin. No studies have yet reported frataxin protein and mRNA levels in a large cohort of FRDA patients, carriers and controls.Methodology/Principal FindingsWe enrolled 24 patients with classic FRDA phenotype (cFA), 6 late onset FRDA (LOFA), all homozygous for GAA expansion, 5 pFA cases who harbored the GAA expansion in compound heterozygosis with FXN point mutations (namely, p.I154F, c.482+3delA, p.R165P), 33 healthy expansion carriers, and 29 healthy controls. DNA was genotyped for GAA expansion, mRNA/FXN was quantified in real-time, and frataxin protein was measured using lateral-flow immunoassay in peripheral blood mononuclear cells (PBMCs). Mean residual levels of frataxin, compared to controls, were 35.8%, 65.6%, 33%, and 68.7% in cFA, LOFA, pFA and healthy carriers, respectively. Comparison of both cFA and pFA with controls resulted in 100% sensitivity and specificity, but there was overlap between LOFA, carriers and controls. Frataxin levels correlated inversely with GAA1 and GAA2 expansions, and directly with age at onset. Messenger RNA expression was reduced to 19.4% in cFA, 50.4% in LOFA, 52.7% in pFA, 53.0% in carriers, as compared to controls (p<0.0001). mRNA levels proved to be diagnostic when comparing cFA with controls resulting in 100% sensitivity and specificity. In cFA and LOFA patients mRNA levels correlated directly with protein levels and age at onset, and inversely with GAA1 and GAA2.Conclusion/SignificanceWe report the first explorative study on combined frataxin and mRNA levels in PBMCs from a cohort of FRDA patients, carriers and healthy individuals. Lateral-flow immunoassay differentiated cFA and pFA patients from controls, whereas determination of mRNA in q-PCR was sensitive and specific only in cFA.

This study hypothesizes that the brain shows hyper connectedness as amyotrophic lateral sclerosis (ALS) progresses. 54 patients (classified as “early stage” or “advanced stage”) and 25 controls underwent magnetoencephalography and MRI recordings. The activity of the brain areas was reconstructed, and the synchronization between them was estimated in the classical frequency bands using the phase lag index. Brain topological metrics such as the leaf fraction (number of nodes with degree of 1), the degree divergence (a measure of the scale-freeness) and the degree correlation (a measure of disassortativity) were estimated. Betweenness centrality was used to estimate the centrality of the brain areas.In all frequency bands, it was evident that, the more advanced the disease, the more connected, scale-free and disassortative the brain networks. No differences were evident in specific brain areas. Such modified brain topology is sub-optimal as compared to controls. Within this framework, our study shows that brain networks become more connected according to disease staging in ALS patients.

Rapid reconfigurations of brain activity support efficient neuronal communication and flexible behaviour. Suboptimal brain dynamics is associated to impaired adaptability, possibly leading to functional deficiencies. We hypothesize that impaired flexibility in brain activity can lead to motor and cognitive symptoms of Parkinson’s 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 relate to 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 correct behaviour.

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The problem of describing how different brain areas interact between each other has been granted a great deal of attention in the last years. The idea that neuronal ensembles behave as oscillators and that they communicate through synchronization is now widely accepted. To this regard, EEG and MEG provide the signals that allow the estimation of such communication in vivo. Hence, phase-based metrics are essential. However, the application of phasedbased metrics for measuring brain connectivity has proved problematic so far, since they appear to be less resilient to noise as compared to amplitude-based ones. In this paper, we address the problem of designing a purely phase-based brain connectivity metric, insensitive to volume conduction and resilient to noise. The proposed metric, named phase linearity measurement (PLM), is based on the analysis of similar behaviors in the phases of the recorded signals. The PLM is tested in two simulated datasets as well as in real MEG data acquired at the Naples MEG center. Due to its intrinsic characteristics, the PLM shows considerable noise rejection properties as compared to other widely adopted connectivity metrics. We conclude that the PLM might be valuable in order to allow better estimation of phase-based brain connectivity.