Fondazione Ospedale San Camillo
Fondazione Ospedale San Camillo
Von Stockum S.,Fondazione Ospedale San Camillo |
Nardin A.,University of Padua |
Schrepfer E.,University of Padua |
Schrepfer E.,Venetian Institute of Molecular Medicine |
And 2 more authors.
Neurobiology of Disease | Year: 2016
Mitochondria are double membrane-bounded organelles residing in the cytoplasm of almost all eukaryotic cells, which convert energy from the disposal of organic substrates into an electrochemical gradient that is in turn converted into ATP. However, the ion gradient that is generated through the oxidation of nutrients, may lead to the production of reactive oxygen species (ROS), which can generate free radicals, damaging cells and contributing to disease. Originally described as static structures, to date they are considered extremely plastic and dynamic organelles. In this respect, mitochondrial dynamics is crucial to prevent potential damage that is generated by ROS. For instance, mitochondria elongate to dilute oxidized proteins into the mitochondrial network, and they fragment to allow selective elimination of dysfunctional mitochondria via mitophagy. Accordingly, mitochondrial dynamics perturbation may compromise the selective elimination of damaged proteins and dysfunctional organelles and lead to the development of different diseases including neurodegenerative diseases.In recent years the fruit fly Drosophila melanogaster has proved to be a valuable model system to evaluate the consequences of mitochondria quality control dysfunction in vivo, particularly with respect to PINK1/Parkin dependent dysregulation of mitophagy in the onset of Parkinson's Disease (PD). The current challenge is to be able to use fly based genetic strategies to gain further insights into molecular mechanisms underlying disease in order to develop new therapeutic strategies.This article is part of a Special Issue entitled: Role of mitochondria in physiological and pathophysiological functions in the central nervous system. © 2015 Elsevier Inc.
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: PHC-26-2014 | Award Amount: 4.35M | Year: 2015
PD_manager aims to build and evaluate an innovative, mhealth, patient centric ecosystem for Parkinsons disease (PD) management. The analysis of experts diagnostic behaviour and the decomposition of tasks undertaken by the various actors during the disease management will enable the validation of technology against routine clinical judgment measures . Primary motor symptoms such as tremor, bradykinesia and postural imbalance and non-motor symptoms, such as sleep, speech and cognitive disorders, will be evaluated with data captured by light, unobtrusive, co-operative, mobile devices: sensor insoles, a wristband and the patients or caregivers (the role of which is of paramount importance) smartphone. Data mining studies will lead to the implementation of a Decision Support Platform with suggestions for modifications in the medication which is the key for prolongation of independence and improved Quality of Life. Compliance with medical recommendations will also be studied; the patient will be motivated to adhere to his medication and diet, will be empowered to exercise and make physiotherapies and will be educated about occupational and speech therapy in order to self-manage his condition. The PD_manager Knowledge Management platform will be built with a cloud-based, open architecture approach based on FI-WARE that will support the use of any commercial set of sensors within the Internet of Things concept. The successful implementation of all abovementioned objectives will be evaluated in a total of 230 patients (the 30 that will be enrolled at the first phase of the project and 200 more during the pilot). In addition to the evaluation of the clinical effectiveness, acceptability and usability of the developed platform and mobile apps a detailed study for the potential of PD_manager as a new care model in terms of health outcomes, quality of life, care efficiency gains and economic benefits will also be conducted.
Stankovic I.,University of Belgrade |
Krismer F.,Innsbruck Medical University |
Jesic A.,University of Novi Sad |
Antonini A.,Fondazione Ospedale San Camillo |
And 14 more authors.
Movement Disorders | Year: 2014
Consensus diagnostic criteria for multiple system atrophy consider dementia as a nonsupporting feature, despite emerging evidence demonstrating that cognitive impairments are an integral part of the disease. Cognitive disturbances in multiple system atrophy occur across a wide spectrum from mild single domain deficits to impairments in multiple domains and even to frank dementia in some cases. Frontal-executive dysfunction is the most common presentation, while memory and visuospatial functions also may be impaired. Imaging and neuropathological findings support the concept that cognitive impairments in MSA originate from striatofrontal deafferentation, with additional contributions from intrinsic cortical degeneration and cerebellar pathology. Based on a comprehensive evidence-based review, the authors propose future avenues of research that ultimately may lead to diagnostic criteria for cognitive impairment and dementia associated with multiple system atrophy. © 2014 International Parkinson and Movement Disorder Society.
Franciotti R.,University of Chieti Pescara |
Delli Pizzi S.,University of Chieti Pescara |
Perfetti B.,University of Chieti Pescara |
Tartaro A.,University of Chieti Pescara |
And 6 more authors.
Movement disorders : official journal of the Movement Disorder Society | Year: 2015
BACKGROUND: Studying default mode network activity or connectivity in different parkinsonisms, with or without visual hallucinations, could highlight its roles in clinical phenotypes' expression. Multiple system atrophy is the archetype of parkinsonism without visual hallucinations, variably appearing instead in Parkinson's disease (PD). We aimed to evaluate default mode network functions in multiple system atrophy in comparison with PD.METHODS: Functional magnetic resonance imaging evaluated default mode network activity and connectivity in 15 multiple system atrophy patients, 15 healthy controls, 15 early PD patients matched for disease duration, 30 severe PD patients (15 with and 15 without visual hallucinations), matched with multiple system atrophy for disease severity. Cortical thickness and neuropsychological evaluations were also performed.RESULTS: Multiple system atrophy had reduced default mode network activity compared with controls and PD with hallucinations, and no differences with PD (early or severe) without hallucinations. In PD with visual hallucinations, activity and connectivity was preserved compared with controls and higher than in other groups. In early PD, connectivity was lower than in controls but higher than in multiple system atrophy and severe PD without hallucinations. Cortical thickness was reduced in severe PD, with and without hallucinations, and correlated only with disease duration. Higher anxiety scores were found in patients without hallucinations.CONCLUSIONS: Default mode network activity and connectivity was higher in PD with visual hallucinations and reduced in multiple system atrophy and PD without visual hallucinations. Cortical thickness comparisons suggest that functional, rather than structural, changes underlie the activity and connectivity differences. © 2015 International Parkinson and Movement Disorder Society.
Agency: European Commission | Branch: FP7 | Program: CP-FP | Phase: HEALTH-2007-3.1-6 | Award Amount: 2.75M | Year: 2009
Our comprehensive approach to clinical continuity by integrated care (IC) across the secondary-primary interface departs from a preliminary literature review selecting frequent chronic conditions (CC) as stroke, COPD and HF as our focus areas. However, within each of these areas IC is a small activity, still, requiring more basic research. As IC for these different CC are based on the same patient values (feeling safe, participation and primary feedback) the synergistic effect from cross-sectional relationships arising from this project should be significant. In all, our 11 deliverables may be important to trespass the critical mass required for an expansion of this kind of IC as far as justified by the empirical results. In general, moderately improved health at minimal costs might be expected from some point of their life to a large segment of the population in EU suffering from the CC in study. That would deliver goodwill to the EU! Special projects are going to investigate the relevance of the access to health improvements by these Low-Tech-IC-interventions in low- and middle-income MS with distinct problems of fragmented care systems. The project has several milestones: 1) A kick-off Symposium aiming to establish a common decision-making framework introducing the HTA method 2) A systematic literature review checking preliminary choices of focus areas after 6 months 3) After 18 months a comprehensive status of the progress of the different trials and surveys is scheduled with respect to both timeliness and scientific content 4) After 30 months the practical IC-guides for clinicians on stroke, heart failure and COPD, respectively, should be concluded after an extensive hearing in an international network related to the 2nd Annual meeting of the consortium. 5) After 36 months the final reporting and dissemination of an HTA of IC should provide the top level of clinical, administrative and political decision-makers with a solid base for progressive decision-making. In conclusion, a meso-strategy for dissemination of IC in EU with formation of a country-specific, multidisciplinary network of specialists in the involved fields as corner-stone for setting up new clinical implementations and recommendations for adaptation of financial and organisation conditions.
Agency: European Commission | Branch: FP7 | Program: MC-IAPP | Phase: FP7-PEOPLE-2011-IAPP | Award Amount: 1.73M | Year: 2012
Biological signals recorded from the human body can be translated into actions of external devices to create man-machine interaction. This concept has clinical implications in rehabilitation technologies for replacing or recovering impaired motor functions. Among the possible biosignals for man-machine interaction (brain, nerve, and muscle signals), muscle signals, i.e. electromyography (EMG), are the only that allow applications in routine clinical use within a commercially reasonable time horizon. Although the current efforts in myoelectric interfaces are mainly focusing on decoding EMG signals, myoelectric interaction has the unique and little exploited feature of provoking changes in the neural circuits that are active during the interaction, i.e. of artificially inducing brain plasticity. However, current commercially viable myoelecric interfaces do not implement sensory-motor integration (decoding intentions and at the same time providing a sensory feedback to the patient), which conversely is the basis of plasticity of the central nervous system. This limit reflects the gap between academic research and the clinical and commercial needs. Myoelectric interfacing with sensory-motor integration is indeed feasible now if the knowledge from basic neurophysiology research and signal analysis in the academia is transferred to industrial sectors and if the requirements of and testing for clinical and commercial viability are transferred from the industry to academia. With a consortium of internationally regarded European academic teams and industries, we thus propose the implementation of sensory-motor integration into commercially viable myoelectric devices in two key clinical applications: 1) training for the active control of prostheses; and 2) rehabilitation of stroke patients with robotics. These two areas require a similar technological ground for sensory-motor integration and for artificial induction of neural plasticity, necessary to (re)learn motor tasks.
Biundo R.,Fondazione Ospedale San Camillo |
Calabrese M.,NeuroLogica |
Weis L.,Fondazione Ospedale San Camillo |
Facchini S.,Fondazione Ospedale San Camillo |
And 3 more authors.
PLoS ONE | Year: 2013
Background:Cognitive deficits may occur early in Parkinson's disease (PD) but the extent of cortical involvement associated with cognitive dysfunction needs additional investigations. The aim of our study is to identify the anatomical pattern of cortical thickness alterations in patients with early stage PD and its relationship with cognitive disability.Methods:We recruited 29 PD patients and 21 healthy controls. All PD patients performed an extensive neuropsychological examination and 14 were diagnosed with mild cognitive impairment (PD-MCI). Surface-based cortical thickness analysis was applied to investigate the topographical distribution of cortical and subcortical alterations in early PD compared with controls and to assess the relationship between cognition and regional cortical changes in PD-MCI.Results:Overall PD patients showed focal cortical (occipital-parietal areas, orbito-frontal and olfactory areas) and subcortical thinning when compared with controls. PD-MCI showed a wide spectrum of cognitive deficits and related significant regional thickening in the right parietal-frontal as well as in the left temporal-occipital areas.Conclusion:Our results confirm the presence of changes in grey matter thickness at relatively early PD stage and support previous studies showing thinning and atrophy in the neocortex and subcortical regions. Relative cortical thickening in PD-MCI may instead express compensatory neuroplasticity. Brain reserve mechanisms might first modulate cognitive decline during the initial stages of PD. © 2013 Biundo et al.
Gava P.,University of Padua |
Kern H.,Ludwig Boltzmann Institute of Electrical Stimulation and Physical Rehabilitation |
Carraro U.,Fondazione Ospedale San Camillo
Experimental Aging Research | Year: 2015
Background/Study Context: The capacity to perform everyday tasks is directly related to the muscular power the body can develop (see Appendix). The age-related loss of power is a fact, but the characterization or the rate of muscle power loss remains an open issue. Data useful to study the decline of the skeletal muscles power are largely available from sources other than medical tests, e.g., from track and field competitions of Masters athletes. The aim of our study is to identify the age-related decline trend of the power developed by the athletes in carrying out the track and field events.Methods: Absolute male world records of 16 events were collected along with world records of male Masters categories. Performance was normalized with respect to the absolute record; the performance of various age groups is consequently represented by a number ranging from 1 (world absolute records) to 0 (null performance). The performance of a jumping event is transformed into a parameter proportional to the power developed by the athletes: the displacement of the center of gravity of the athlete. Throwing events are further normalized for the decreasing weight of the implements with the increasing age of the Masters athletes.Results: Most track and field events show a linear decline to 70 years. The annual rate of power decline for all the events (running, throwing, and jumping), using a simplified synthesis, is 1.25% per year. The events that involve mostly upper limbs (shot put, javelin throw) show a higher rate of decline (1.4% per year) compared to those where the lower limbs are mostly involved (long jump 1.1%, track events 0.6-0.7% per year). This analysis of muscle power decline is only partially in line with the results of works based on clinical tests. A clarification of the reasons for such discrepancy may provide clinically significant information.Conclusion: Human power decline in Masters athletes was analyzed, adopting a coherent approach based on an extended database. Skeletal muscle power starts declining after the age of 30, with slight variations depending on the events. This conclusion is in line with only some of the previous studies. The various trend lines point to 0 at the age of 110 years, which is in line with the present human survival age. The study can be further developed with a suitable database for male and female Masters performances to facilitate longitudinal studies, which are currently lacking. © 2015 Taylor and Francis Group, LLC.
PubMed | University of Padua, Venetian Institute of Molecular Medicine and Fondazione Ospedale San Camillo
Type: | Journal: Neurobiology of disease | Year: 2016
Mitochondria are double membrane-bounded organelles residing in the cytoplasm of almost all eukaryotic cells, which convert energy from the disposal of organic substrates into an electrochemical gradient that is in turn converted into ATP. However, the ion gradient that is generated through the oxidation of nutrients, may lead to the production of reactive oxygen species (ROS), which can generate free radicals, damaging cells and contributing to disease. Originally described as static structures, to date they are considered extremely plastic and dynamic organelles. In this respect, mitochondrial dynamics is crucial to prevent potential damage that is generated by ROS. For instance, mitochondria elongate to dilute oxidized proteins into the mitochondrial network, and they fragment to allow selective elimination of dysfunctional mitochondria via mitophagy. Accordingly, mitochondrial dynamics perturbation may compromise the selective elimination of damaged proteins and dysfunctional organelles and lead to the development of different diseases including neurodegenerative diseases. In recent years the fruit fly Drosophila melanogaster has proved to be a valuable model system to evaluate the consequences of mitochondria quality control dysfunction in vivo, particularly with respect to PINK1/Parkin dependent dysregulation of mitophagy in the onset of Parkinsons Disease (PD). The current challenge is to be able to use fly based genetic strategies to gain further insights into molecular mechanisms underlying disease in order to develop new therapeutic strategies. This article is part of a Special Issue entitled: Role of mitochondria in physiological and pathophysiological functions in the central nervous system.
Biundo R.,Fondazione Ospedale San Camillo |
Weis L.,Fondazione Ospedale San Camillo |
Pilleri M.,Fondazione Ospedale San Camillo |
Facchini S.,Fondazione Ospedale San Camillo |
And 3 more authors.
Journal of Neural Transmission | Year: 2013
Prevalence of mild cognitive impairment (MCI) in Parkinson's disease (PD) is variable likely due to methodological differences in classification criteria and lack of consensus about neuropsychological tests used for cognitive profiling. The main objective of our study was to identify the most suitable neuropsychological tests and determine their screening and diagnostic cutoff scores for PD-MCI. A series of 104 consecutive PD patients performed an extensive neuropsychological evaluation. Individual test values were converted into Z-scores using relative published normative data. According to published criteria, PD patients were categorized as PD-CNT (PD without cognitive impairment), PD-MCI (patients performing -1.5 SDs below the mean score in at least one cognitive domain), and PDD. We used receiver operating characteristic (ROC) curves and K-means clustering analyses to calculate the best discriminating power of each neuropsychological tests in detecting PD-MCI. PD patients were categorized as follows: 55 PD-CNT (53 %), 34 PD-MCI (33 %), and 15 PDD (14 %). PD-MCI had lower education, longer disease duration and greater frequency of hallucinations than PD-CNT. We found that only the Trail Making test, Rey-Osterrieth Complex Figure Test (ROCF) copy, Frontal Assessment Battery (FAB), Digit Span Backward, and Rey's word auditory verbal learning test (RVLT) immediate recall reached significant screening and diagnostic validity in predicting PD-MCI (AUC 0.705-0.795) with cutoff scores calculated by ROC analyses lying within normal range for normative data. Specific neuropsychological tests covering verbal memory, attention/set-shifting, and visual-spatial deficits are the best predictors of MCI in PD if valid cutoff scores are used. These results have consequences for cognitive diagnosis and potentially in establishing the rate of PD cognitive decline. © 2013 Springer-Verlag Wien.