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La salute mentale deve essere inserita all’interno di un piano globale d’azione. Queste sono le indicazioni che l’Organizzazione Mondiale della Sanità ha rivolto a tutti gli Stati Membri per il periodo 2013-2020. A tale scopo, la Società Italiana di Psichiatria ha costituito un gruppo di lavoro insieme alle Associazioni di pazienti e familiari e ad altre società scientifiche per stilare la “Carta della Salute Mentale”, che è stata presentata il 12 aprile a Roma presso la Biblioteca del Senato “Giovanni Spadolini”. Durante la giornata sono intervenuti rappresentati del mondo politico, delle Istituzioni, del mondo accademico e delle associazioni di pazienti e familiari per fare il punto sulla gestione del paziente con disturbi mentali.
Il gap tra il tipo di cure di cui i malati psichiatrici avrebbero bisogno e quello che invece ricevono è ancora molto ampio. Mancano ad esempio i dati di prevalenza di molte malattie mentali tra cui la schizofrenia, il disturbo bipolare e i disturbi psichiatrici e comportamentali dell’età evolutiva. “Si sente l’esigenza di una struttura in grado di coniugare ricerca preclinica con valore traslazionale a ricerca clinico-epidemiologica, in grado anche di creare reti - spiega Enrico Alleva - Direttore del Reparto Neuroscienze Comportamentali presso il Dipartimento di Biologia Cellulare e Neuroscienze dell’Istituto Superiore di Sanità (ISS)–. L’ISS vanta diversi filoni di ricerca preclinica che spaziano da studi epidemiologici a studi sulla plasticità neurale attraverso biomarcatori come NGF o BDNF, fino allo studio dei fattori che possono modificare la risposta al trattamento attraverso l’impiego dei Big Data. Presso l’ISS sono attive anche ricerche multidisciplinari focalizzate sui fattori in grado di modificare la suscettibilità a disturbi quali autismo o ADHD. Per quanto riguarda la ricerca clinico-epidemiologica, sono già in corso studi su disturbi del neuro-sviluppo, sindromi ticcose, stadi vegetativi e depressioni maggiori. L’ISS cura inoltre molte attività istituzionali di supporto al Ministero della Salute oltre alle attività di formazione e informazione degli operatori del Sistema Sanitario Nazionale.
Nuovo approccio integrato della Società Italiana di Psichiatria: PRESENTAZIONE UFFICIALE DELLA “CARTA DELLA SALUTE MENTALE”
12 Aprile 2017 Senato della Repubblica, Roma
Nel 1948 la prima Assemblea mondiale della salute (World Health Assembly) decide di istituire una giornata dedicata della salute in tutto il mondo. Dal 1950 la giornata mondiale della salute (World Health Day) si celebra dunque il 7 aprile, per ricordare la fondazione dell’Oms avvenuta il 7 aprile 1948. Ogni anno viene scelto per la giornata un tema specifico, che evidenzia un’area di particolare interesse per l’Oms.
La giornata è un’occasione per promuovere a livello globale la sensibilizzazione su argomenti cruciali di salute pubblica di interesse della comunità internazionale, e lanciare programmi a lungo termine sugli argomenti al centro dell’attenzione. La giornata mondiale della salute non è quindi un evento che si riduce ai lavori di un giorno, ma è ogni volta il punto di partenza di un percorso mirato a migliorare le condizioni di salute in tutto il mondo.
7 Aprile 2017 Giornata Mondiale della salute - DEPRESSIONE: PARLIAMONE
Adverse events such as abuse in childhood are closely related to risk of psychiatric disorder in adulthood. But the effects of such experiences are modulated by genetic factors. Can we begin to understand the daunting complexity of this interaction by looking at the stress hormone system, which is often dysregulated in psychiatric disorders?
The glucocorticoid receptor is a nuclear receptor which engenders a transcriptome-wide stress response in the cell. It is now clear that exposure to the stress hormone also remodels the epigenetic landscape, mostly through a decrease in DNA methylation.
Such changes, which (among other possible effects) had implications for neuronal differentiation were evident even after a washout period of twenty days. Effects were long lasting and seem capable of altering the impact of subsequent adverse stress-related events over a lifetime.
Basic molecular mechanisms are a good place to start when trying to understand complex gene-environment interactions
Such insights prompted work on multipotent human hippocampal progenitor cells. These cells react to glucocorticoids and so may represent a good model of early exposure to stress. In this model, exposure to dexamethasone produced the expected epigenetic changes in DNA methylation.
Importantly, these changes were found to be located in gene enhancer regions that are relevant both to brain development and to risk of mood disorders. Demethylation seems to prime genes to be more reactive to future stress.
But genetic variation modulates the epigenetic response to glucocorticoid activation and to changes in transcription. And it is revealing that SNPs linked by genome-wide association studies to increased risk of schizophrenia and depression are found in the loci showing methylation changes. This association may show – at a molecular level – how the risk of stress-related disorders is determined by both environmental and genetic factors.
There are certainly many non-glucocorticoid mechanisms that influence an individual’s vulnerability or resilience to mental health problems, Professor Binder concluded. But glucocorticoids do seem able to prime an organism to respond differently to stress.
Polygenic risk factors interact with the environment to increase vulnerability to depression. Do molecular events caused by exposure to stress hormones help us understand this complex interaction?
Adverse events such as abuse in childhood are closely related to risk of psychiatric disorder in adulthood. But the effects of such experiences are modulated by genetic factors. Can we begin to understand the daunting complexity of this interaction by looking at the stress hormone system, which is often dysregulated in psychiatric disorders?
The glucocorticoid receptor is a nuclear receptor which engenders a transcriptome-wide stress response in the cell. It is now clear that exposure to the stress hormone also remodels the epigenetic landscape, mostly through a decrease in DNA methylation.
Such changes, which (among other possible effects) had implications for neuronal differentiation were evident even after a washout period of twenty days. Effects were long lasting and seem capable of altering the impact of subsequent adverse stress-related events over a lifetime.
Basic molecular mechanisms are a good place to start when trying to understand complex gene-environment interactions
Such insights prompted work on multipotent human hippocampal progenitor cells. These cells react to glucocorticoids and so may represent a good model of early exposure to stress. In this model, exposure to dexamethasone produced the expected epigenetic changes in DNA methylation.
Importantly, these changes were found to be located in gene enhancer regions that are relevant both to brain development and to risk of mood disorders. Demethylation seems to prime genes to be more reactive to future stress.
But genetic variation modulates the epigenetic response to glucocorticoid activation and to changes in transcription. And it is revealing that SNPs linked by genome-wide association studies to increased risk of schizophrenia and depression are found in the loci showing methylation changes. This association may show – at a molecular level – how the risk of stress-related disorders is determined by both environmental and genetic factors.
There are certainly many non-glucocorticoid mechanisms that influence an individual’s vulnerability or resilience to mental health problems, Professor Binder concluded. But glucocorticoids do seem able to prime an organism to respond differently to stress.
Polygenic risk factors interact with the environment to increase vulnerability to depression. Do molecular events caused by exposure to stress hormones help us understand this complex interaction?
Adverse events such as abuse in childhood are closely related to risk of psychiatric disorder in adulthood. But the effects of such experiences are modulated by genetic factors. Can we begin to understand the daunting complexity of this interaction by looking at the stress hormone system, which is often dysregulated in psychiatric disorders?
The glucocorticoid receptor is a nuclear receptor which engenders a transcriptome-wide stress response in the cell. It is now clear that exposure to the stress hormone also remodels the epigenetic landscape, mostly through a decrease in DNA methylation.
Such changes, which (among other possible effects) had implications for neuronal differentiation were evident even after a washout period of twenty days. Effects were long lasting and seem capable of altering the impact of subsequent adverse stress-related events over a lifetime.
Basic molecular mechanisms are a good place to start when trying to understand complex gene-environment interactions
SNPs interact with early trauma to predict mood and anxiety disorders
Such insights prompted work on multipotent human hippocampal progenitor cells. These cells react to glucocorticoids and so may represent a good model of early exposure to stress. In this model, exposure to dexamethasone produced the expected epigenetic changes in DNA methylation.
Importantly, these changes were found to be located in gene enhancer regions that are relevant both to brain development and to risk of mood disorders. Demethylation seems to prime genes to be more reactive to future stress.
But genetic variation modulates the epigenetic response to glucocorticoid activation and to changes in transcription. And it is revealing that SNPs linked by genome-wide association studies to increased risk of schizophrenia and depression are found in the loci showing methylation changes. This association may show – at a molecular level – how the risk of stress-related disorders is determined by both environmental and genetic factors.
There are certainly many non-glucocorticoid mechanisms that influence an individual’s vulnerability or resilience to mental health problems, Professor Binder concluded. But glucocorticoids do seem able to prime an organism to respond differently to stress.
Polygenic risk factors interact with the environment to increase vulnerability to depression. Do molecular events caused by exposure to stress hormones help us understand this complex interaction?