New molecule to fight cognitive decline

Article by SoLongevity Research
Science has been working for a long time to understand the causes of aging and find new therapies to counteract, or at least delay, the most damaging effects on the body. A new study from the Graduate Center of New York, for example, has just identified one of the mechanisms involved in cognitive decline that accompanies old age. The research, published in Nature Communications, reveals the role played by a molecule called ten-eleven-translocation 1 (or TET 1) in promoting the myelination of brain connections (axons), a process essential to maintain a healthy central nervous system, which is progressively compromised by ageing or affected by neurodegenerative diseases, such as Alzheimer’s and multiple sclerosis.

Science is working to understand the causes of brain aging and find therapies to counteract its deleterious effects

The brain fixes itself

As we age, however, myelin production gradually declines, leading to cognitive decline and dementia when neurons are no longer able to communicate effectively. Identifying, and if possible reversing, the processes that limit myelin production is therefore a promising way to combat the cognitive effects of aging. And it is from this consideration that the new research stems. Rete neuronale con attività elettrica delle cellule neuronali TET 1 appears to be involved in the production of the myelin sheath that covers the axons of neurons, without which signal conduction is interrupted

Rejuvenate your brain

“Abbiamo ideato una serie di esperimenti per identificare quali molecole possono influenzare il ringiovanimento del cervello”, spiega Sarah Moyon, prima autrice del nuovo studio. “È così che abbiamo scoperto che i livelli di TET 1 diminuiscono progressivamente nel cervello dei topi anziani, e questo compromette la capacità di modificare l’espressione genica per produrre nuova mielina funzionante”.  Utilizzando tecniche di bionformatica e dati genomici, il gruppo di ricerca è riuscito a dimostrare che nei roditori giovani TET 1 induce delle modifiche epigenetiche nel Dna (cioè delle alterazioni dell’espressione genica che non sono legate a mutazioni strutturali) che risultano fondamentali per garantire la produzione di mielina e la trasmissione di informazioni tra neuroni. Un’attività che risulta probabilmente compromessa negli esemplari anziani: modificando geneticamente i topi per esprimere una versione non funzionante di TET 1 nei progenitori degli oligodendrociti, i ricercatori hanno infatti constatato che questi non riuscivano più a produrre mielina funzionante, con il risultato che i topi, seppur anagraficamente giovani, esibivano un comportamento tipico di esemplari ben più anziani.  Researchers at the Graduate Center of New York hypothesize that in the elderly, myelin production decreases due to altered TET 1 activity

TET 1 is a molecule that promotes myelination of neuronal axons

“The tracked age-related decline in TET 1 activity could explain the inability to produce new myelin in the brains of older people,” comments Patrizia Casaccia, director of the Neuroscience Initiative at the Graduate Center of New York. “I also believe that by studying the effects of ageing in both healthy people and individuals with neurodegenerative diseases, it will help us to develop new therapies with which to slow, or stop altogether, the progression of devastating diseases such as multiple sclerosis and Alzheimer’s.”

TET 1 appears to hold promise for the development of therapies to rejuvenate the brain and treat neurodegenerative diseases

Researchers believe the discovery could open the door to new therapeutic strategies aimed at rejuvenating the brain and improving cognitive ability in the elderly population. Further trials are already planned, with researchers attempting to increase TET 1 levels in the brains of elderly mice to see if this will promote better myelin production and reverse age-related cognitive decline.

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