Epilessia: una nuova strategia per ridurre le crisi

Pubblicato sul  “Journal of Neuroscience”uno studio che vede tra gli autori Sacha Genovesi e Yuri Bozzi del CIBIO dell’Università di Trento

[ Foto Alessio Coser per Università di Trento]

L’epilessia è un disturbo neurologico cronico. Chi ne soffre è esposto al rischio di attacchi epilettici ricorrenti, che possono presentarsi nell’arco della vita in vari modi a seconda dell'età e della parte del cervello coinvolta. In Europa ne sono colpite in media otto persone su mille. Ad aggravare la frequenza degli attacchi epilettici in pazienti affetti da epilessia cronica possono essere anche eventi infiammatori acuti scatenati da comuni infezioni.

Uno studio, che vede tra gli autori Sacha Genovesi e Yuri Bozzi del Centro di Biologia integrata CIBIO dell’Università di Trento, ed i ricercatori del gruppo di Matteo Caleo dell’Istituto di Neuroscienze del CNR di Pisa, ha dimostrato per la prima volta il ruolo chiave di una proteina della famiglia delle chemochine, chiamata CCL2, nell’insorgenza delle crisi di epilettiche scatenate da infiammazione acuta. Lo studio apre la strada alla sperimentazione di nuove terapie contro l’epilessia.

«Finora – spiegano Bozzi e Caleo – si sapeva che le crisi epilettiche aumentano la produzione di CCL2 nel cervello oltre che nel sangue, ma non si sapeva che questa molecola fosse tra quelle che stimolano l’insorgenza di crisi epilettiche. Il nostro studio dimostra che CCL2 ha un effetto scatenante e che bloccando la produzione e
l’azione di questa molecola nel cervello siamo in grado di ridurre il numero e la frequenza di crisi epilettiche che insorgono in seguito ad infiammazione. Per bloccare questa molecola possiamo ricorrere a farmaci già disponibili sul mercato o sperimentare dei nuovi farmaci specifici».

L’articolo dei ricercatori sugli effetti scatenanti della chemochina CCL2 è stato pubblicato il 31 marzo sulla rivista americana “Journal of Neuroscience” con il titolo “The chemokine CCL2 mediates the seizure enhancing effects of systemic inflammation” (ovvero “La chemochina CCL2 regola l’insorgenza delle crisi epilettiche scatenate
dall’infiammazione sistemica”). Lo studio è stato condotto in collaborazione con l’azienda farmaceutica Angelini, che ha fornito il bindarit, una molecola della ricerca Angelini capace di inibire la produzione di CCL2. Come autori “senior” vengono indicati Matteo Caleo (ricercatore dell’Istituto di Neuroscienze del CNR) e Yuri Bozzi.

Ufficio stampa Unitn

01/04/2016

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