Another important genetic discovery related to alpha-synuclein was that the mutation known as PARK4 was actually a triplication of the normal SNCA gene, meaning that people with PARK4 had extra copies of the gene and thus, an excess of normal alpha-synuclein. So, too much alpha-synuclein — and not just an abnormal form of the protein — can cause Parkinson’s, albeit in very few people. Partly because of this discovery, much research in the last decade has focused at the molecular level on the mechanisms by which the alpha-synuclein protein contributes to the death of dopamine neurons. It is now understood as one of three elements within the dopamine neuron — the other two are dopamine and calcium — that interact to cause neurodegeneration.