New Study Attempts to Interrupt Parkinson's Disease

Studies and efforts to stop chronic neurodegenerative diseases never cease. As new discoveries are used to diagnose patients, the level of severity is also a main target of continued research. Among these, there are also many studies being done to slow the progression of Parkinson’s disease.

According to a study published in the journal Science, a group of scientists from Northwestern University were able to identify a specific toxic cascade that causes neuronal degeneration in people suffering from Parkinson’s disease. The difference between this research and others is that the group of Northwestern scientists found a way to interrupt said toxic cascade.

The same study showed that a certain antioxidant can help significantly pause the evolution of the disease when implemented during its early stages. Antioxidants have the ability to break the degenerative cycle triggered by Parkinson’s disease as well as improve neuronal functioning.

These results are a breath of fresh air for people suffering from this disease since it is a starting point for the development of new therapies. This research and what it means for human neurons is critically important for advancing solutions.

The study began six years ago in Massachusetts at a lab run by Dr. Dimitri Krianc, and the last four years of it were completed at Northwestern’s Feinberg School of Medicine. Dimitri Krianc, a professor at the Aaron Montgomery Ward, was the senior author and person in charge of the study. Lena Burbulla was another author on the project as well as Krianc’s fellow colleague. Taking into account that death occurred in this neurodegenerative disease due to the intervention of toxins, the two developed combative treatments using antioxidants. They used human neurons to determine whether these antioxidants could stop the degenerative process of the disease. Ultimately, their study showed this method of treatment can in fact delay or even outright stop Parkinson’s progression. From these results, it is possible to start new research towards a definite cure.

Parkinson’s disease is the second most common neurodegenerative disease around today. In this condition, the neurons in the part of the brain that contains dopamine and controls motor actions die. As people age, they tend to lose dopamine neurons. However, in the case of Parkinson’s, the loss of dopamine neurons is too large and the remaining ones cannot compensate for it.

It is important to understand why the dopamine neurons die; only then can proper treatment be determined. According to previous studies done by Krianc and his team, mitochondria and lysosomes cause cell death. This occurs due to the accumulation of a protein called alpha-synuclein and oxidized dopamine. They noted that the build-up of oxidized dopamine was caused by the activity of an enzyme called lysosomal glucocerebrosidase, and thus the overall lysosomal function was weakened, causing the neurons to be destroyed.

The oxidized dopamine interferes with the lysosomes and damages the neurons’ mitochondria by increasing mitochondrial oxidant stress, resulting in an increase in the level of oxidized dopamine. This then creates a cyclic state of degeneration. According to Krianc, the mitochondrial and lysosomal interferences are two critical pathways in the development of the disease. Once the team became aware of the toxic cascade of neurons, they were able to find ways to interrupt it. Lowering the oxidized dopamine and improving the mitochondrial oxidant stress were the key strategies in all their experiments, said Krianc. The team did this using antioxidants. According to Krianc, the downstream toxic effects could be attenuated and even completely prevented in human dopaminergic neurons with this approach. The team’s results bring new hope to the continuing struggle against Parkinson’s.