Purché non sia straziante – “Quant’è bella giovinezza che si fugge tuttavia!”. E’ il primo verso dei Canti della “Canzona da Bacco”, scritta da Lorenzo il Magnifico, poeta, mecenate, banchiere e signore della Firenze rinascimentale. Una ballata che ci ricorda l’ineluttabilità del trascorrere del tempo del quale potremmo usufruirne più a lungo e in buone condizioni di salute.
Coleen Murphy, professoressa di Biologia molecolare presso l’Università di Princeton (Usa), ha analizzato lo stato della ricerca sull’invecchiamento e delle sue ragioni biologiche, pubblicando i risultati in “How We Age”, un testo recensito su “Nature”. Negli studi effettuati, gli scienziati hanno utilizzato due minuscoli invertebrati, il “Caenorhabditis elegans” (un verme lungo un millimetro che vive nel suolo delle regioni temperate) e la “Drosophila melanogaster” (il moscerino della frutta). Si tratta di “organismi modello” per la ricerca scientifica, in particolare per le neuroscienze, la genetica, l’immunologia, il metabolismo e l’invecchiamento. I risultati sono applicabili agli “organismi modello” dei vertebrati come i topi e anche agli esseri umani. Una scoperta fondamentale è stata quella della mutazione di un gene (Daf-2) di “Caenorhaditis elegans” che ha permesso ai vermi di vivere più del doppio del normale, a patto che un altro gene (daf-16) fosse attivo. I geni
“Daf-2 e Daf-16 agiscono insieme per salvaguardare il verme quando le condizioni sono difficili o il cibo scarseggia, innescando una serie di meccanismi protettivi. La mutazione del primo gene (Daf-2) prolunga la vita attivando processi cellulari protettivi come il controllo di qualità delle proteine e disattivando l’attività metabolica dannosa. Analogamente, i risultati della ricerca sono adattabili alla “Drosophila melanogaster”, e alle mutazioni di un gene umano equivalente al Daf-16.
Le analisi hanno evidenziato che l’invecchiamento è un processo flessibile sul quale è possibile intervenire anche con i farmaci. La professoressa Murphy ha delineato un’ampia gamma di fattori biologici che possono influenzare la durata della vita, tra cui il danno al Dna e le modificazioni epigenetiche, cioè i cambiamenti molecolari che influenzano l’espressione genica senza alterare la sequenza del Dna. “In gioventù “l’espressione dei geni” è strettamente regolata, ma questi meccanismi di controllo sbagliano durante l’invecchiamento”, ha affermato la professoressa Murphy.
I costituenti cellulari, in particolare le proteine, possono diventare troppo scarsi o troppo abbondanti, il che può impedire alla cellula di funzionare normalmente. Le mutazioni genetiche che combattono gli effetti dell’invecchiamento e le misure relative allo stile di vita favoriscono i processi cellulari positivi.
“I meccanismi molecolari che rendono benefica la dieta e l’esercizio fisico sono sempre più compresi e alcuni di questi sono gli obiettivi dei farmaci”, ha concluso la professoressa Murphy. I ricercatori sperano di utilizzare questi rimedi per ottenere gli stessi benefici di uno stile di vita sano. Insomma, in un futuro non troppo lontano si potrà vivere oltre i 120 anni.
Primo Mastrantoni, presidente comitato scientifico di Aduc
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