1,721,056 research outputs found
Physical and sports activity during the COVID-19 pandemic
No full textThe SARS-COVID 19 pandemic, which has hit the planet in recent times, in addition to changing daily life
habits, also has negative repercussions on indoor exercise and sports, due to the social restrictions imposed by
governments to address and contain the contagion. As a first response to this change in the social habits of
practicing indoor physical activity in gyms, physical activity and sports professionals have developed innovative
and original design ideas for outdoor training by proposing different physical disciplines for different classes of
users. However, knowledge of the state of the art relating to the adaptations and opinions of physical activity and
sports clients following the closure of indoor gyms is still poor. Considering that this knowledge differs from
territory to territory by type of social and environmental context, the problem of the study is limited to the
territory of interest and towards which the attention of indoor gym managers is directed. The chosen area is that
of the municipality of Fisciano (province of Salerno) where the users of the Studio Zen gym are interested,
which has about 100 customers. The aim of the study is to quantify the level of participation in outdoor training
activities organized in compliance with the anti-COVID legislation, paying particular attention to the effects of
constraints on physical and sports practice. The study was conducted using the Cluster Analysis methodology
which, through the administration of a questionnaire drawn up with the Google Forms platform, collected data
relating to the level of motor and sports practice before and after the closure of the indoor gyms. The data
collected show that the outdoor training proposal in this study did not have a high level of participation for
various reasons, both subjective and objective, which led the subjects to choose other training methods or decide not to perform any motor or sports activity
Stress responses in down syndrome neurodegeneration: State of the art and therapeutic molecules
Full text linkDown syndrome (DS) is the most common genomic disorder characterized by the increased incidence of developing early Alzheimer’s disease (AD). In DS, the triplication of genes on chromosome 21 is intimately associated with the increase of AD pathological hallmarks and with the development of brain redox imbalance and aberrant proteostasis. Increasing evidence has re-cently shown that oxidative stress (OS), associated with mitochondrial dysfunction and with the failure of antioxidant responses (e.g., SOD1 and Nrf2), is an early signature of DS, promoting protein oxidation and the formation of toxic protein aggregates. In turn, systems involved in the surveil-lance of protein synthesis/folding/degradation mechanisms, such as the integrated stress response (ISR), the unfolded stress response (UPR), and autophagy, are impaired in DS, thus exacerbating brain damage. A number of pre-clinical and clinical studies have been applied to the context of DS with the aim of rescuing redox balance and proteostasis by boosting the antioxidant response and/or inducing the mechanisms of protein re-folding and clearance, and at final of reducing cognitive decline. So far, such therapeutic approaches demonstrated their efficacy in reverting several aspects of DS phenotype in murine models, however, additional studies aimed to translate these approaches in clinical practice are still needed
Shining a light on defective autophagy by proteomics approaches: implications for neurodegenerative illnesses
No full textIntroduction: Autophagy is one of the most conserved clearance systems through which eukaryotes manage to handle dysfunctional and excess organelles and macromolecules. This catabolic process has not only a role in the maintenance of basal turnover of cellular components, but it is also essential in cells adaptation to stress conditions. In the last decades, defects in autophagic machinery have been identified as a feature in neurodegenerative diseases. In this context, mass spectrometry-based proteomics has become an important tool in the comprehensive analysis of proteins involved in the autophagic flux. Area covered: In this review, we discuss recent contributions of proteomic techniques in the study of defective autophagy related to neurodegenerative illness. Particular emphasis is given to the identification of i) shared autophagic markers between different disorders, which support common pathological mechanisms; ii) unique autophagic signature, which could aid to discriminate among diseases. Expert opinion: Proteomic approaches are valuable in the identification of alterations of components to the autophagic process at different steps of the process. The investigation of autophagic defects associated with neurological disorders is crucial in order to unravel all the potential mechanism leading to neurodegeneration and propose effective therapeutic strategies targeting autophagy
Buxus in Europe: Late quaternary dynamics and modern vulnerability.
No full textThe suggested location of broadleaved evergreen trees in Europe during the last full-glacial has traditionally
favoured a southerly refugial model, which proposes survival in the Mediterranean peninsulas
and recolonization of central and northern Europe during the Holocene. This hypothesis is not always
substantiated by thorough reviews of original past and modern occurrence data, or considered in the
light of plant traits and autoecology. Our approach focuses on the genus Buxus with the aim of exploring
(i) the relationship between the location of refugia and post-glacial population dynamics, (ii) past
processes determining density, fragmentation and local extinctions of modern populations, and (iii) the
vulnerability of Buxus in the context of the undergoing environmental changes. We compiled a database
of over 3600 modern occurrences and 676 fossil sites to reconstruct the distribution of Buxus in Europe
since 30 ka cal BP. The location of fossil finds and the plant traits of Buxus indicate that it persisted widely
across its modern distribution through the last glacial period with modes varying from region to region.
The E Pyrenees, W Alps, and Jura Mts hosted dense populations, which expanded exponentially during the
whole Holocene, and resulted in a modern continuous distribution area. In contrast, the Mediterranean
Peninsulas hosted sparse populations, which increased exponentially only during the first half of the
Holocene, clearly decreased in the last 4.5 ka BP and resulted in a highly fragmented modern distribution
area, most likely in relation to the climate trends towards dry conditions of the last few millennia. These
results challenge the common view that the Mediterranean regions are the exclusive and most important
refuge areas for evergreen broadleaved trees and stress the importance of considering long-term population
dynamics based on fossil data to evaluate the vulnerability of modern fragmented plant populations
in view of conservation actions.
© 2012 El
Redox imbalance and metabolic defects in the context of Alzheimer disease
No full textRedox reactions play a critical role for intracellular processes, including path- ways involved in metabolism and signaling. Reactive oxygen species (ROS) act either as second messengers or generators of protein modifications, funda- mental mechanisms for signal transduction. Disturbance of redox homeostasis is associated with many disorders. Among these, Alzheimer’s disease is a neu- rodegenerative pathology that presents hallmarks of oxidative damage such as increased ROS production, decreased activity of antioxidant enzymes, oxi- dative modifications of macromolecules, and changes in mitochondrial homeo- stasis. Interestingly, alteration of redox homeostasis is closely associated with defects of energy metabolism, involving both carbohydrates and lipids, the major energy fuels for the cell. As the brain relies exclusively on glucose metabolism, defects of glucose utilization represent a harmful event for the brain. During aging, a progressive perturbation of energy metabolism occurs resulting in brain hypometabolism. This condition contributes to increase neu- ronal cell vulnerability ultimately resulting in cognitive impairment. The cur- rent review discusses the crosstalk between alteration of redox homeostasis and brain energy defects that seems to act in concert in promoting Alzhei- mer’s neurodegeneration
From redox proteomics to clinical practice: Search for therapeutic targets
No full textAlzheimer disease (AD) is the most common form of dementia in the elderly population, characterized by a gradual deterioration of memory and other cognitive functions. The major pathological characteristics of AD brains are the presence of senile plaques, made of amyloid β-peptide (Aβ), neurofibrillary tangles, composed of hyperphosphorylated tau protein, and neuronal loss. Among putative mechanisms responsible of neurodegeneration, several studies demonstrated the role of oxidative stress as an important factor contributing to the initiation and progression of AD. If from one side disruption of redox balance and increased production of free radicals are likely to be related to mitochondria dysfunction and/or aberrant accumulation of misfolded proteins, on the other side the abnormal accumulation of Aβ and tau proteins appears to promote the redox imbalance. In addition, evidence has suggested that oxidative stress may augment the production and aggregation of Aβ and facilitate the phosphorylation and polymerization of tau, thus forming a vicious cycle that promotes the initiation and progression of AD. Taken together, these findings suggest that therapeutic strategies aimed at preventing/reducing oxidative stress-mediated damage may be effective for the treatment of AD and other neurodegenerative disorders
mTOR in Alzheimer Disease and Its Earlier Stages: Links to Oxidative Damage in the Progression of this Dementing Disorder
No full textAlzheimer’s disease (AD) is the most prevalent form of dementia in the elderly population and has worldwide impact. The etiology of the disease is complex and results from the confluence of multiple mechanisms ultimately leading to neuronal loss and cognitive decline. Among risk factors, aging is the most relevant and accounts for several pathogenic events that contribute to disease-specific toxic mechanisms. Accumulating evidence linked the alterations of the mammalian target of rapamycin (mTOR), a serine/threonine protein kinase playing a key role in the regulation of protein synthesis and degradation, to age-dependent cognitive decline and pathogenesis of AD. To date, growing studies demonstrated that aberrant mTOR signaling in the brain affects several pathways involved in energy metabolism, cell growth, mitochondrial function and proteostasis. Recent advances associated alterations of the mTOR pathway with the increased oxidative stress. Disruption of all these events strongly contribute to age-related cognitive decline including AD. The current review discusses the main regulatory roles of mTOR signaling network in the brain, focusing on its role in autophagy, oxidative stress and energy metabolism. Collectively, experimental data suggest that targeting mTOR in the CNS can be a valuable strategy to prevent/slow the progression of AD
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