A similarity between two distinct neurodegenerative diseases, Parkinson’s and Alzheimer’s, may lead to a potential new drug treatment for Parkinson's. On a biochemical level, the diseases develop when sticky proteins form clumps in brain cells, researchers from Emory Health Sciences said. They found that the same enzyme also spurred the process in both diseases.

In a new study published online in Nature Structural and Molecular Biology, Emory researchers explain how they used this similarity between Parkinson’s and AD to develop a drug that stops tau proteins from becoming sticky and therefore prevents them from clumping together. Although still in its research phase, this would theoretically prevent the onset of AD, as a similar version of it has prevented Alzheimer’s disease in animal studies. The next step is to test on animals the Parkinson’s version of a drug to inhibit the enzyme to see if these positive results can be repeated.

Read: Parkinson’s Disease Treatment Reverses Symptoms In Mice, Increases Dopamine Receptors

"In Parkinson's, alpha-synuclein behaves much like Tau in Alzheimer's," said study lead research Keqiang Ye, in a statement. "We reasoned that if [the enzyme] AEP cuts Tau, it's very likely that it will cut alpha-synuclein too."

The discovery, though promising, is likely not the ultimate cure for Parkinson's, as AEP, the enzyme it inhibits, is not the only enzyme that leads to toxic build-up of proteins. Still, the implication of this treatment could have many far-reaching benefits.

According to the Parkinson’s Disease Foundation, Parkinson’s is a chronic and progressive disease that specifically affects a patient's movements; about one million Americans live with the disease. Parkinson's develops very slowly, and some of the earliest symptoms may include a tremor or uncontrolled shaking of a limb or of the hands, The Mayo Clinic reported. Other symptoms include slowed movement, rigid muscles, impaired posture and balance, loss of automatic movements, such as the ability to blink or smile, speech changes, and writing changes.

While the exact cause of the disease is not known, doctors believe there are both genetic and environmental factors at play in an individual's personal risk. The condition is linked to malfunction and death of neurons in the brain that produce dopamine, a hormone associated with movement and coordination. As more neurons are destroyed, a person’s dopamine levels gets lower and lower. As a result, they continually lose the ability to control their movement. More serious complications of Parkinson’s disease include thinking difficulties, depression, swallowing difficulties, sleep problems, bladder problems, and constipation.

There have been a number of recent innovations in the treatment of Parkinson’s disease. For example, earlier this year, scientists were able to improve and even reverse the symptoms of Parkinson’s in mice by using small molecules to reprogram existing brain cells to take over the job of brain cells destroyed by the disease. Once again, this research has yet to be done on humans, but together with the new study, recent findings are promising for both those with Parkinson’s disease and their loved ones.

Source: Zhang Z, Kang SS, Liu X, et al. Asparagine endopeptidase cleaves α-synuclein and mediates pathologic activities in Parkinson's disease. Nature Structural and Molecular Biology. 2017

Correction: This article has been corrected to show that currently about one million Americans live with Parkinson's Disease.

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