Alpha–synuclein is a 140 amino acid protein and its physiological function so far is not clear, however it is suspected to play a role in synaptic plasticity. In addition alpha–synuclein interferes with different intracellular signal transduction pathways related to oxidative stress and apoptosis. This protein is the main constituent of Lewy bodies which are the pathological hallmark of Parkinson's disease but are also frequent in other neurodegenerative disorders including Alzheimer's disease (AD). Different papers are supporting a toxic gain of function of Alpha–synuclein oligomers or aggregates. Over–expression and some point–mutations of Alpha–synuclein are increasing the tendency to form aggregates, but also environmental factors like oxidative stress are promoting fibril information. It has been shown that Beta–synuclein, a member of the same protein family can counteract abnormal Alpha–synuclein aggregation in different in vitro and in vivo experiments. This property seems to be related to the N–terminal sequence of Beta–synuclein. A peptide library with a manifold of variations of this sequence was synthesized. Peptides were synthesised, modified and tested in several cell free assays and cell experiments. In vivo the influence of some of the peptides was evaluated in hAPP transgenic mice testing learning and memory behaviour and investigating changes in brain morphology. Several peptides displayed pronounced neuroprotective effects in tissue culture models of chronic and acute neurodegeneration. Protective effects seem to be unrelated to a direct interaction with protein aggregation, leading to the assumption that these sequences are triggering important protective functions, what is in agreement with reports about a direct interaction of Beta–synuclein with the Akt – pathway. Stabilized small peptides have been also investigated in an animal model of AD, influencing cognitive function and at the same way reducing amyloid dependent pathology. In spite of the fact that the mechanism behind these effects remains unclear, data are indicating that synuclein derived peptides might be the basis for development of efficacious treatment strategies for different neurodegenerative disorders. Currently the exploration of the mechanisms of action are further targets of investigation, with specific focus on mechanisms counteracting neuronal apoptosis and pathways involved with protection against oxidative stress.