Elucidating the Alsin structure to function relationships toward a better understanding of Infantile-onset ascending hereditary spastic paralysis and possible therapeutic strategies.

Infantile onset ascending hereditary spasticity (IAHSP) is an hereditay neurodegenerative disease which affects children since first age of life, causing progressive ascending paralysis of limbs. Researchers have found that specific genetic mutations are cause of this pathology. Genes are manuals that our cells use to build proteins, fundamental gears for the functioning of the human body. Errors into the instructions results in an incorrect build of this gears, malfunctioning and thus to pathological condition. The aim of this project is to observe the effects (at the the molecular scale) of the gene traduction in proteins the machines that develop all physiological functions. When a protein is not correctly printed it may work in a wrong way causing a pathology. In this work we aim at obtaining a model to investrigate differences between the physiological and mutated (i.e., pathological) version of the Alsin protein. Our computational modelling activity allows to have a very high investigation resolution and allows to test the protein behaviour in several virtual experiments which may also involve the presence of drugs.  In a greater detail we will virtually test a huge number of drugs and their affinity to the alsin protein and we will chose the best candidates for further experimental studies.