Unveiling the molecular correlates of early synaptic dysfunction in Alzheimer’s disease

Synapses are structures that allow the neurons to be connected and store memories. Synapses are perturbed in very early stages of Alzheimer’s disease. Nonetheless, previous studies in animals models have been carried out at late stages of the disease, where the ongoing pathogenic processes are very complex, making it difficult to understand the initial triggers of the disease. Currently, there is no cure for Alzheimer’s disease and recent clinical trials failed. My project will improve our basic knowledge on synaptic dysfunction during the early stages of the disease. My preliminary data indicates that the mouse model I am using shows perturbed synaptic function. This makes it a good platform to further elucidate pathogenic mechanisms underlying synapse dysfunction and how this leads to impaired brain homeostasis. This approach will provide new insights into the molecular players of the early cascade of AD and reveal new candidate genes to be investigated as potential therapeutic targets for the pre-clinical phase of AD