Parkinson's disease, an extremely debilitating disease of dopamine neurons, has remained a mystery for many years. However, recent studies in genetics and models have shown that defects in pathways in neuronal cells cause a large build up of many damaged cellular products and structures, causing neuronal death. In addition to these intracellular factors, it was proposed and tested in mice that prion-like spreading of rogue transporter proteins causes the rapid acceleration of the pathology of Parkinson's.
The above genes are the focus for therapeutic alternatives to the management of PD. Not only are these genes analyzed for errors, but the corresponding enzymes that catalyze reactions or chaperone proteins are also being studied for the regulation of the above gene mutations. In particular, the genes that code for extracellular communication and transport protein, alpha-synuclein fibril, are of the utmost interest due to their prion-like tendencies in widespread neuronal death. Altering the dysfunction and build up of alpha-synuclein fibril may be the key to alleviating the progression of PD.