Giving neurons a second youth: Leticia Peris's approach to combating Alzheimer's disease

In Alzheimer's disease, amyloid and tau proteins accumulate abnormally and alter internal structures of neurons, compromising their architecture and communication at synapses. Leticia Peris is seeking to understand how these proteins act together: ‘We started from the idea that Alzheimer's disease is a disease of the neuronal cytoskeleton and, in this context, we wanted to understand how the pathogenic effects of amyloid and Tau proteins combine.’

Funded by the Alzheimer's Foundation, her team's work has already shown that amyloid proteins make microtubules too rigid, preventing the maintenance of dendritic spines, which are essential for synaptic communiation. Tau protein exacerbates the problem by disrupting both microtubules and another key structure: actin. As a result, synapses weaken and disappear, accelerating the loss of neuronal connections.

To counter this process, Leticia Peris is exploring a promising approach: rejuvenating microtubules by returning them to a more “youthful” form, known as tyrosinated microtubules. 
‘If we could rejuvenate cytoskeletons using drugs, we could make synapses more resistant to the toxic effects of amyloid and Tau proteins. This project could pave the way for new treatments for Alzheimer's disease that could protect memory and cognitive functions,’ concludes the researcher.