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HOME > Epilessia e autismo hanno un gene alterato in comune che può essere “corretto”
Epilessia e autismo hanno un gene alterato in comune che può essere “corretto”
Epilessia e autismo hanno un gene alterato in comune. Inoltre, il gene, in quanto molecola, può essere “corretto” con un farmaco. È la scoperta avvenuta grazie ad uno studio coordinato da Maria Giuseppina Miano, ricercatrice dell’Istituto di genetica e biofisica Adriano Buzzati-Traverso del Consiglio nazionale delle ricerche (Cnr-Igb) di Napoli.
La ricerca, finanziata da Fondazione Telethon, è stata pubblicata su ‘Human Molecular Genetics’.
Le malattie genetiche dello sviluppo del cervello, dalle encefalopatie epilettiche ai disturbi nello spettro autistico, sono un insieme di patologie diverse che tuttavia condividono una serie di segni clinici comuni che vanno dai disturbi nell’apprendimento a quelli del comportamento.
Il nuovo studio ha identificato un legame anche genetico tra questi disturbi. Si tratta di un percorso in cui vie molecolari diverse arrivano a una stessa molecola bersaglio, che risponde con una specifica reazione.
La ricerca del Cnr-Igb ha individuato gli effetti dei danni che tale via di convergenza genetica manifesta in alcune forme di malattie del neurosviluppo.
Inoltre ha sperimentato un possibile intervento farmacologico, rivelatosi efficace in modelli di patologia generati in laboratorio.
Al centro dello studio, il gene bersaglio Kdm5c. Sono le sue mutilazioni, infatti, ad essere responsabili di uno spettro di patologie neurologiche pediatriche, quali disabilità intellettiva, epilessia e autismo.
Questo gene codifica un regolatore della condensazione della cromatina, complesso di proteine e Dna in cui è organizzato il genoma.
“Il nostro studio ha dimostrato che mutazioni in geni regolatori dell’espressione del gene Kdm5c, anch’essi coinvolti in disturbi del neurosviluppo, innescano una serie di difetti a carico di geni che esercitano un ruolo chiave nella fase di maturazione del cervello – spiega Miano -. Grazie a questa ricerca oggi sappiamo che diversi geni neuronali, finora ritenuti responsabili di patologie distinte, fanno parte di uno stesso network molecolare all’interno del quale il gene Kdm5c funziona da collegamento genetico”.
Nuove prospettive
Lo studio in questione apre nuove prospettive alla comprensione del malfunzionamento dei network genetici convergenti.
La ricerca infatti ha portato anche ad altri risultati. “Abbiamo dimostrato, attraverso l’utilizzo di modelli cellulari e animali, che il gene è una molecola che può cioè essere agganciata da un farmaco che ne corregge la ridotta espressione – prosegue la ricercatrice – Grazie alla collaborazione con il collega Elia Di Schiavi dell’Istituto di bioscienze e biorisorse (Cnr-Ibbr), è stato possibile ‘ricreare’ il difetto a carico del gene Kdm5c nel Caenorhabditis elegans, un piccolo animale invertebrato che, sebbene sia molto distante dall’uomo, possiede geni con una funzione simile. In particolare, siamo riusciti a dimostrare che utilizzando l’acido idrossamico suberoilanilide è possibile correggere il ridotto dosaggio di Kdm5c, recuperando così funzioni che sono alla base dei processi di maturazione di classi di neuroni danneggiati in molti disturbi del neurosviluppo”.
Per la prima volta, quindi, si può definire il ruolo di un marcatore-malattia adatto allo sviluppo di terapie di precisione dirette a colpire specifiche funzioni danneggiate.
FONTI:
www.si24.it
www.adnkronos.com
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