Furthermore, alterations in the expression pattern of genes associated with synaptic function in the Thy1-aSyn mice are consistent with recent evidence indicating that excessive SNCA causes deficits in neurotransmitter release by inhibiting synaptic vesicle reclustering after endocytosis [41]; such alterations may lead to derangements at the synapses evident by the inhibition of neurotransmitter release which may impair synaptic plasticity, cause behavioral changes and contribute to neurodegeneration and eventually clinical PD. The gene discussed is THY1; the disease is Parkinson disease.