Archives Italiennes De Biologie最新文献

The Montreal Cognitive Assessment (MoCA) is a rapid screening tool, including subtests to assess several cognitive domains, developed to detect MCI from normal ageing cognitive changes. Several validation and normative studies have conducted around the world considering the influences of age and education on the MoCA score, but none takes into account the lifestyle and habits. However, lifestyles, and particularly physical activity (PA) have been positively associated with both physical and mental health in elderly. The aim of the present study is to investigate the influence of regularly practiced PA on the MoCA scores in a sample of Italian healthy elderly males. For this purpose sixty-five healthy adult males, aged 65-81 years were assigned to two groups, physically active group (PAG, N=33), and sedentary group (SG, N=32), according to recommended levels of physical activity by the World Health Organization. The Italian version of MoCA was administered to each participant. Raw data were analysed by a multiple regression model in which the independent variables were PA, age and education. Results showed a highly significant influence of PA on MoCA total score and on several cognitive domain sub-scores. Furthermore, multiple regression analysis indicated a larger impact on scores by PA than both age and education. In the light of these findings, it is advisable to pay attention to the life style of subject that undergoing a neuropsychological evaluation like the MoCa and in particular the level of PA practiced, as well as age and education.

Exercise may exert beneficial effects on cognitive functions and play an important role in the prevention of neurodegenerative diseases. Such effects seem to be mediated by changes in anti-oxidative status, but limited information is available on the nature of molecular pathways supporting the antioxidant effects of exercise in the brain. In this study 3-5-month-old male Wistar albino rats were subjected to three times/week moderate intensity exercise on a rodent treadmill for a period of 6 weeks. The tissue antioxidant activity towards various reactive oxygen species (ROS) was determined in the hippocampus. In addition, to identify the molecular pathways that may be involved in ROS metabolism, the expression of nerve growth factor (NGF) and sirtuins (SIRT1 and SIRT3) were measured. Our results showed a higher antioxidant activity in the hippocampus of physically trained rats compared to sedentary controls. Furthermore, exercise induced an up-regulation of NGF, possibly related to an improved redox balance in the hippocampus. These results suggest that physical exercise might prevent age-induced oxidative damage in the hippocampus.

DM1 is an autosomal-dominant disorder characterized by muscle weakness, myotonia, and multisystemic involvement. According to current literature fatigue and daytime sleepiness are among the main symptoms of DM1. Oxidative stress has been proposed to be one of the pathogenic factors of fatigue consequent to DM1. In this study, we investigated the dimensions of experienced fatigue and  physiological fatigue in a sample of 26 DM1 patients (17 males, 9 females, mean age 41.6 years, SD±12.7); experienced fatigue has been studied through Fatigue Severity Scale (FSS), and physiological fatigue was measured through an intermittent incremental exercise of the forearm muscles using a myometer; oxidative stress balance markers trend during aerobic exercise test have been collected. The occurrence of central fatigue in the sample means that central activation worsens during the motor contraction; interestingly FSS score was significantly correlated to MVC (before and after the effort, r-before=-0.583, p<0.01, r-after= -0.534, p<0.05), and to motor disability measured by MRC (r=-0.496, p<0.05); moreover we found a strong tendency towards significance in the association to lactate baseline (r=0.378, p=0.057).Results are discussed to define whether or not, based on clinical and laboratory grounds, such exercise training protocol may be suitable for proper management of DM1 patients; proper assessment of fatigue should be included in algorithms for data collection in DM1 patient registries.

A common pathological feature of neurodegenerative disorders (NDs), such as Alzheimer's (AD) and Parkinson's (PD) diseases, is the abnormal accumulation and misfolding of specific proteins, primarily α-synuclein (α-syn), β-amyloid1-42 (Aβ) and tau, in brain and in peripheral tissues too. Oxidative stress has been proved to be involved in NDs at various levels and, in particular, in such protein alterations, on the contrary physical activity is emerging as a counteracting factor in NDs. In the present work, the content of Aβ, α-syn and tau in red blood cells (RBCs) derived from ten endurance athletes (ATHL) and ten sedentary volunteers (SED) were compared before and after in vitrooxidative stress treatment. Total Aβ, α-syn and tau were quantified in RBCs (isolated from the subjects) by immunoenzymatic assays. Oxidative stress was induced by in vitro H₂O₂ administration to RBCs. H₂O₂ treatment was confirmed to significantly enhance ROS accumulation in RBCs. Total Aβ content in RBCs was lower in the ATHL subgroup with respect to the SED one. In the SED subgroup, but not in the ATHL one, total Aβ levels were increased by oxidative stress. Total α-syn content was lower in the ATHL subgroup with respect to the SED one and α-syn levels were increased by oxidative stress in both subgroups, with the percentage of increase higher in SED. Total tau content was comparable in both ATHL and SED and it was not affected by oxidative stress. Our data confirm previous findings evidencing that both oxidative stress and sedentary style contribute to aberrant folding and accumulation of NDs-related proteins, pointing to the importance of both anti-oxidant therapies and exercising in the prevention and treating of such diseases.

We investigated the relationship between length and dreamlike quality in sleep mentation reports. Reports were obtained by waking subjects at sleep onset (SO) and at 5 and 10 minutes into the second (REMP2) and fourth REM periods (REMP4). Reports were recorded, transcribed, and scored blindly for total word count (TWC) and dreamlike quality as measured by a composite dream scale score (CDS). Dreamlike quality was strongly correlated with TWC; both CDS and TWC scores increased across successively later awakenings. Significant differences were found in both TWC and CDS between SO and REMP4 and also between REMP2 and REMP4; however, differences were not significant between SO and REMP2 or between the 5 and 10 minute awakenings in REMPs 2 and 4. These findings provide further evidence that the amount of dreamlike mentation is related to the within-sleep arousal level rather than to REMP duration and that the dreamlike quality of reports increases as they become longer.

The paratympanic organ (PTO) is a sensory organ located in the medial wall of the tympanic cavity of birds. The organ looks like a small tapering vesicle, and is equipped with a sensory epithelium formed by supporting cells (SCs) and Type II hair cells (Type II-HCs). The function of the PTO has not yet been precisely defined. The prevailing current hypothesis is that the PTO assesses the air pressure exerted on the external surface of the tympanic membrane. The PTO could may thus function as a barometer and, in flying birds, also as an altimeter. The afferent synapses of the PTO of chicken were described in detail in a previous paper. Reciprocal synapses between efferent nerve endings (ENEs) and the HCs were also observed, suggesting the existence of local microcircuits. The aim of this work was to provide a more detailed ultrastructural description of these microcircuits in the PTO of chicken. We observed for the first time: (1) reciprocal synapses between the HCs and the afferent nerve endings (ANEs); (2) presence of two distinct types of ENEs; (3) reciprocal synapses between the HCs and both types of ENEs. Overall, these results indicate that a complex processing of the incoming sensory signals may occur in the PTO. This thus suggests that the PTO may perform more complex functions than those supposed until now. We hypothesize that the PTO could have a role in the low-frequency sound perception.

The cellular prion protein (PrPc) is physiologically expressed within selective brain areas of mammals. Alterations in the secondary structure of this protein lead to scrapie-like prion protein (PrPsc), which precipitates in the cell. PrPsc has been detected in infectious, inherited or sporadic neurodegenerative disorders. Prion protein metabolism is dependent on autophagy and ubiquitin proteasome. Despite not being fully elucidated, the physiological role of prion protein relates to chaperones which rescue cells under stressful conditions.Methamphetamine (METH) is a widely abused drug which produces oxidative stress in various brain areas causing mitochondrial alterations and protein misfolding. These effects produce a compensatory increase of chaperones while clogging cell clearing pathways. In the present study, we explored whether METH administration modifies the amount of PrPc. Since high levels of PrPc when the clearing systems are clogged may lead to its misfolding into PrPsc, we further tested whether METH exposure triggers the appearance of PrPsc. We analysed the effects of METH and dopamine administration in PC12 and striatal cells by using SDS-PAGE Coomassie blue, immune- histochemistry and immune-gold electron microscopy. To analyze whether METH administration produces PrPsc aggregates we used antibodies directed against PrP following exposure to proteinase K or sarkosyl which digest folded PrPc but misfolded PrPsc. We fond that METH triggers PrPsc aggregates in DA-containing cells while METH is not effective in primary striatal neurons which do not produce DA. In the latter cells exogenous DA is needed to trigger PrPsc accumulation similarly to what happens in DA containing cells under the effects of METH. The present findings, while fostering novel molecular mechanisms involving prion proteins, indicate that, cell pathology similar to prion disorders can be mimicked via a DA-dependent mechanism by a drug of abuse.

Brain connectivity is associated to behavioral states (e.g. wake, sleep) and modified by physical activity although, to date, it is not clear which components (e.g. hypothalamus-pituitary-adrenal axis hormones, cytokines) associated to the exercise are involved. In this pilot study, we used extreme exercise (UltraTriathlon) as a model to investigate physical-activity-related changes of brain connectivity. We studied post-race brain synchronization during wakefulness and sleep as well as possible correlations between exercise-related cytokines/hormones and synchronization features. For wakefulness, global synchronization was evaluated by estimating from fMRI data (12 athletes) the brain global connectivity (GC). GC increased in several brain regions, mainly related to sensory-motor activity, emotional modulation and response to stress that may foster rapid exchange of information across regions, and reflect post-race internally-focused mental activity or disengagement from previous motor programs. No significant correlations between cytokines/hormones and GC were found. For sleep (8 athletes), synchronization was evaluated by estimating the local-(cortical) and global-related (thalamo- cortical) EEG features associated to the phenomenon of Sleep Slow Oscillations (SSO) of NREM sleep. Results showed that: power of fast rhythms in the baseline preceding the SSO increased in midline and parietal regions; amplitude and duration of SSOs increased, mainly in posterior areas; sigma modulation in the SSO up state decreased. In the post race, IL-10 positively correlated with fast rhythms baseline, SSO rate and positive slope; IL-1ra and cortisol inversely correlated with SSO duration; TNF-α and C-reactive protein positively correlated with fast rhythm modulation in the SSO up state. Sleep results suggest that: arousal during sleep, estimated by baseline fast rhythms, is increased; SSO may be sustained by cortical excitability, linked to anti-inflammatory markers (IL-10); thalamo-cortical entrainment, (sigma modulation), is impaired in athletes with higher inflammatory markers.