1,721,282 research outputs found
Psicologia del multitasking
No full textTelefonate, e-mail, messaggi, documenti digitali, news on line: gli uffici si stanno trasformando in maniera sempre più prepotente nella palestra dove allenarsi a gestire attività multiple accompagnate da interruzioni continue. L'ingresso delle tecnologie informatiche nella vita quotidiana e soprattutto nei luoghi di lavoro rende il multitasking una condizione onnipresente, di cui tutti abbiamo esperienza. Ma quante e quali attività differenti siamo in grado di gestire? Come influisce il multitasking sulle prestazioni lavorative e sui vissuti soggettivi? E' cognitivamente sostenibile
Interruzioni spontanee nella gestione dei compiti multipli
No full textE’ stato ampiamente dimostrato come interrompere momentaneamentel'esecuzione di un compito (primario) per svolgerne un altro (secondario)influisca sensibilmente sulla prestazione complessiva, ma anche sulla noia esullo sforzo percepito (Bayley e Konstan, 2006). Si è anche potuto stabilireche durante lo svolgimento di un compito, il carico cognitivo non è costante,bensì presenta un andamento caratterizzato da punti di alto workload e dibasso workload. Questi ultimi sembrano essere tutti coincidenti con le zone diconfine tra le sotto unità che compongono il compito (subtask boundaries)(Bailey e Iqbal, 2008).Obiettivo di questo studio è di verificare se i soggetti, lasciati liberi di deciderequando interrompersi durante l'esecuzione di un compito per eseguirne unosecondario, utilizzino spontaneamente i momenti di basso workload o seadottino strategie alternative
Palmitoylethanolamide (PEA) as a Potential Therapeutic Agent in Alzheimer's Disease
No full textN-Palmitoylethanolamide (PEA) is a non-endocannabinoid lipid mediator belonging to the class of the N-acylethanolamine phospolipids and was firstly isolated from soy lecithin, egg yolk, and peanut meal. Either preclinical or clinical studies indicate that PEA is potentially useful in a wide range of therapeutic areas, including eczema, pain, and neurodegeneration. PEA-containing products are already licensed for use in humans as a nutraceutical, a food supplement, or a food for medical purposes, depending on the country. PEA is especially used in humans for its analgesic and anti-inflammatory properties and has demonstrated high safety and tolerability. Several preclinical in vitro and in vivo studies have proven that PEA can induce its biological effects by acting on several molecular targets in both central and peripheral nervous systems. These multiple mechanisms of action clearly differentiate PEA from classic anti-inflammatory drugs and are attributed to the compound that has quite unique anti(neuro) inflammatory properties. According to this view, preclinical studies indicate that PEA, especially in micronized or ultramicronized forms (i.e., formulations that maximize PEA bioavailability and efficacy), could be a potential therapeutic agent for the effective treatment of different pathologies characterized by neurodegeneration, (neuro) inflammation, and pain. In particular, the potential neuroprotective effects of PEA have been demonstrated in several experimental models of Alzheimer's disease. Interestingly, a single-photon emission computed tomography (SPECT) case study reported that a mild cognitive impairment (MCI) patient, treated for 9 months with ultramicronized-PEA/luteolin, presented an improvement of cognitive performances. In the present review, we summarized the current preclinical and clinical evidence of PEA as a possible therapeutic agent in Alzheimer's disease. The possible PEA neuroprotective mechanism(s) of action is also described
Differential Effects of Palmitoylethanolamide against Amyloid-β Induced Toxicity in Cortical Neuronal and Astrocytic Primary Cultures from Wild-Type and 3xTg-AD Mice
Full text linkBACKGROUND:
Considering the heterogeneity of pathological changes occurring in Alzheimer's disease (AD), a therapeutic approach aimed both to neuroprotection and to neuroinflammation reduction may prove effective. Palmitoylethanolamide (PEA) has attracted attention for its anti-inflammatory/neuroprotective properties observed in AD animal models.
OBJECTIVE AND METHODS:
We evaluated the protective role of PEA against amyloid-β42 (Aβ42) toxicity on cell viability and glutamatergic transmission in primary cultures of cerebral cortex neurons and astrocytes from the triple-transgenic murine model of AD (3xTg-AD) and their wild-type littermates (non-Tg) mice.
RESULTS:
Aβ42 (0.5 μM; 24 h) affects the cell viability in cultured cortical neurons and astrocytes from non-Tg mice, but not in those from 3xTg-AD mice. These effects were counteracted by the pretreatment with PEA (0.1 μM). Basal glutamate levels in cultured neurons and astrocytes from 3xTg-AD mice were lower than those observed in cultured cells from non-Tg mice. Aβ42-exposure reduced and increased glutamate levels in non-Tg mouse cortical neurons and astrocytes, respectively. These effects were counteracted by the pretreatment with PEA. By itself, PEA did not affect cell viability and glutamate levels in cultured cortical neurons and astrocytes from non-Tg or 3xTg-AD mice.
CONCLUSION:
The exposure to Aβ42 induced toxic effects on cultured cortical neurons and astrocytes from non-Tg mice, but not in those from 3xTg-AD mice. Furthermore, PEA exerts differential effects against Aβ42-induced toxicity in primary cultures of cortical neurons and astrocytes from non-Tg and 3xTg-AD mice. In particular, PEA displays protective properties in non-Tg but not in 3xTg-AD mouse neuronal cultured cells overexpressing Aβ
Farmaci del Sistema Nervoso Centrale. Farmaci per il trattamento del Parkinson.
No full textNel capitolo sono elencati i farmaci utilizzati per il trattamento del Morbo di Parkinson
Inhibitory cholinergic control of endogenous GABA release from electrically stimulated cortical slices and K(+)-depolarized synaptosomes
No full textIn the present study we characterize the optimal experimental conditions under which to investigate the cholinergic regulation of endogenous electrically evoked γ-aminobutyric acid (GABA) release from guinea pig cortical slices. Superfusion with the neuronal GABA reuptake inhibitor, SKF89976A (10 μM) caused cortical GABA release to be linearly correlated with the frequency of electrical stimulation (5, 10, 20 Hz). Electrically evoked GABA release (10 Hz) was tetrodotoxin-sensitive and Ca2+-dependent and was under GABAB autoreceptor control. Under these experimental conditions, acetylcholine (0.1–10 μM) and physostigmine (30 μM) decreased the electrically evoked GABA release while the M2 receptor antagonist AFDX-116 (0.01–0.1 μM) counteracted these effects. Similar results were also observed in a cortical synaptosomal preparation stimulated with K+ (10 mM). These findings demonstrate an inhibitory cholinergic regulation of electrically evoked GABA release via M2 receptors located on cortical GABAergic terminals
Changes in gamma-aminobutyric acid release induced by topical administration of drugs affecting its metabolism and receptors: Studies in freely moving guinea pigs with epidural cups
No full textThe effect of local application of drugs affecting gamma-aminobutyric acid metabolism and receptors on cortical aminoacid release has been investigated in freely-moving guinea pigs equipped with epidural cups. Topical treatment with gamma-aminobutyric acid reuptake and/or metabolism inhibitors (alone and in combination) produced a slow and progressive increase in cortical aminoacid release. The inhibition of gamma-aminobutyric acid-transaminase with ethanolamino-O-sulphate seemed to be a suitable procedure for enhancing the gamma-aminobutyric acid efflux without interfering with its auto-receptor-mediated negative feedback, tested with the gamma-aminobutyric acid agonist (±)baclofen and antagonist phaclofen. A substantial part of the gamma-aminobutyric acid outflowing from the cortex was of neuronal origin since tetrodotoxin halved the basal efflux in the presence of gamma-aminobutyric acid reuptake and/or metabolism inhibitors. These results, considered together, indicate that the epidural cup technique may be a useful approach to study changes in cortical gamma-aminobutyric acid release induced by drugs acting on gabaergic transmission and directly applied on the surface of the cortex
Astrocytic palmitoylethanolamide pre-exposure exerts neuroprotective effects in astrocyte-neuron co-cultures from a triple transgenic mouse model of Alzheimer's disease
No full textPalmitoylethanolamide (PEA) is an endogenous lipid mediator that, also by blunting astrocyte activation, demonstrated beneficial properties in several in vitro and in vivo models of Alzheimer's disease (AD). In the present study, we used astrocyte-neuron co-cultures from 3xTg-AD mouse (i.e. an animal model of AD) cerebral cortex to further investigate on the role of astrocytes in PEA-induced neuroprotection. To this aim, we evaluated the number of viable cells, apoptotic nuclei, microtubule-associated protein-2 (MAP2) positive cells and morphological parameters in cortical neurons co-cultured with cortical astrocytes pre-exposed, or not, to Aβ42 (0.5 μM; 24 h) or PEA (0.1 μM; 24 h). Pre-exposure of astrocytes to Aβ42 failed to affect the viability, the number of neuronal apoptotic nuclei, MAP2 positive cell number, neuritic aggregations/100 μm, dendritic branches per neuron, the neuron body area, the length of the longest dendrite and number of neurites/neuron in 3xTg-AD mouse astrocyte-neuron co-cultures. Compared to neurons from wild-type (non-Tg) mouse co-cultures, 3xTg-AD mouse neurons co-cultured with astrocytes from this mutant mice displayed higher number of apoptotic nuclei, lower MAP2 immunoreactivity and several morphological changes. These signs of neuronal suffering were significantly counteracted when the 3xTg-AD mouse cortical neurons were co-cultured with 3xTg-AD mouse astrocytes pre-exposed to PEA. The present data suggest that in astrocyte-neuron co-cultures from 3xTg-AD mice, astrocytes contribute to neuronal damage and PEA, by possibly counteracting reactive astrogliosis, improved neuronal survival. These findings further support the role of PEA as a possible new therapeutic opportunity in AD treatment
Trasmissione catecolaminergica
No full textSono descritti i principi base della trasmissione catecolaminergica ed i recettori adrenergici. Inoltre, sono descritti gli usi terapeutici dei farmaci interagenti con la trasmissione catecolaminergic
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