Synaptic failure is believed to be an important cause of dementia in neurodegenerative diseases like Alzheimer`s disease. Also in Parkinsons`s disease, which starts with motor symptoms, dementia develops in a high number of patients. Due to incredible compensation capacity of the human brain dementia however only become evident when more than half of all synapses are irreversibly lost. Here we aim to understand early changes in synaptic protein synthesis in a mouse model of dementia in Parkinson`s disease. We aim to identify presynaptic changes in the regulation of protein production that alter synaptic function due to the aggregation of the synaptic protein a-synuclein. We intend to discover new synaptic targets for a preventive therapeutical intervention in order to stop synapse loss in time and to identify patients with Parkinsons`s disease at risk to develop dementia early on.