Della serie “infinitamente piccolo, enormemente importante”: quando i recettori hanno un ruolo fondamentale nella cura di una malattia.

La sclerosi multipla è una malattia neurodegenerativa su base flogistica: un attacco da parte del sistema immunitario sulle cellule nervose, che ne provoca la morte con il passare del tempo.

Fino a poco tempo fa, si è sempre pensato che solo il sistema immunitario avesse un ruolo in questo attacco; solo di recente si è visto che, in effetti, vi sono anche gli astrociti tra i protagonisti: essi rilasciano NO che provoca la distruzione del neurone stesso. Nella malattia, infatti, le difese immunitarie del paziente attaccano e distruggono la guaina mielinica che riveste gli assoni neuronali. Il nome stesso della malattia deriva appunto dalle placche cicatriziali che si formano sul midollo o nell’encefalo a causa di questi processi patologici.

Processo patologico sclerosi multiplaOggi però si sono fatti numerosi passi in avanti nello studio di una terapia efficace contro questa malattia, e la cosa più sorprendente è che l’Italia gioca un ruolo centrale in questo: uno studio condotto dal laboratorio di Immunobiologia delle Malattie Neurologiche presso l’Istituto di Neurologia Sperimentale (INSpe), dell’IRCCS Ospedale San Raffaele, ha chiarito le basi cellulari dell’azione neuroprotettiva del composto Fingolimod (Gilenya), immesso in commercio nel 2012 e studiato proprio negli ultimi due anni.

Fingolimod è il capostipite di una nuova classe di farmaci, “modulatori della sfingosina 1-fosfato”: interagisce con i recettori della sfingosina 1-fosfato presenti sui linfociti e sulle cellule del sistema nervoso centrale, bloccando i linfociti nei linfonodi e diminuendo l’attacco degli stessi, che è proprio alla basa della malattia. Il sequestro dei linfociti è reversibile una volta smessa l’assunzione del farmaco. In questo modo, si preserva l’immunità, compresa l’attivazione dei linfociti e la capacità di produrre anticorpi.

Il farmaco può, inoltre, attraversare rapidamente la barriera ematoencefalica e penetrare nel SNC: potrebbe quindi, legandosi ai recettori della S1P, indurre la riparazione e la rimielinizzazione del neurone, limitando l’azione negativa degli astrociti. Di fatto, il farmaco blocca i recettori S1P e quindi il rilascio dello stesso NO.

Dagli studi è emerso che circa il 52% dei pazienti trattati con questo farmaco, hanno evitato ricadute. Messo a confronto con altri farmaci con efficacia simile, è l’unico che non permette la riduzione del volume cerebrale.

Gli effetti collaterali più frequenti sono: cefalea, influenza, mal di schiena, incremento degli enzimi epatici e, meno spesso, riduzione della frequenza cardiaca con blocco atrio-ventricolare (generalmente asintomatici, all’inizio del trattamento) e lieve broncocostrizione.

“Questi risultati evidenziano sempre più il ruolo fondamentale degli astrociti nei processi patologici in atto nelle malattie neurodegenerative, come la sclerosi multipla. Il nostro obiettivo è quello di approfondire ulteriormente lo studio di questa popolazione gliale al fine di raccogliere informazioni necessarie per lo sviluppo di nuove terapie neuroprotettive” spiega Emenuela Colombo, facente parte del team che ha compiuto questo studio.

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