To me this seems unlikely to lead to a cure for Parkinson’s disease (PD). The animal models don’t have PD. They have a lesion in the part of the brain that produces dopamine. This results in the symptoms of PD, but not the actual disease process.

The actual PD disease process is the loss of dopaminergic neurons in the substantia nigra. This neuronal loss is caused by oxidative stress caused by dopamine metabolites. When the excess of released dopamine in not stored in storage vesicles, it is metabolised in oxidative compounds. These oxidation products are damaging the dopaminergic neurons.

In healthy neurons excess dopamine is transported to storage vesicles by alpha-synuclein. Alpha-synuclein is the protein that is the main constituent of Lewy bodies, which are the hallmark of PD.

Alpha-synuclein in the cytosol of dopaminergic neurons needs a ‘chaperone’ to remain in its active unfolded state. Without sufficient chaperones, alpha-synuclein assumes a configuration which is prone to aggregation, resulting in the reduction of bioavailable alpha-synuclein, and thus a reduction in the capacity to transport excess dopamine to storage vesicles. The dopamine that is not stored in these vesicles metabolises in the oxidative compounds that damage the dopaminergic cells.

Countries in which curcuma (turmeric), a chaperone for alpha-synuclein, is part of the daily diet, have a lower incidence of PD, than Western European ones. Curative strategies for PD should aim to develop chaperones for alpha-synuclein.