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Parkinson’s Disease Protein Transmitted Like a Virus
Parkinson’s disease is a slowly progressing neurodegenerative disorder. The symptoms associated with Parkinson’s disease, including trembling, slow movement, and balance problems, occur when dopamine producing cells in the brain are destroyed. It is not known precisely what causes damage to the dopamine producing cells, but most scientists believe that improperly folded proteins are responsible for the disease. These proteins form aggregates, which are called Lewy bodies, that may damage nerve cells, or possibly prevent proper functioning of the nerve cell. Control of symptoms is the main focus of treatment for patients with Parkinson’s disease. Most treatments involve improving motor functions, through medication and exercise programs. Because each patient may experience different symptoms during different stages of Parkinson’s disease, individualized treatment is required. Parkinson’s disease affects many people, with approximately fifty to sixty thousand Americans being diagnosed each year, so effective treatments would be beneficial to the population in general.

A protein called alpha synuclein has been suggested previously to play a role in the development of Parkinson’s disease. The alpha synuclein protein is highly expressed in structures called Lewy bodies, which are protein aggregates associated with the development of Parkinson’s disease. Alpha synuclein aggregates from Lewy bodies have been shown to be transmitted from one cell to another, thus spreading the disease into other nearby neural cells.

It is not understand how these aggregates can be spread to other cells, and what effect this movement has on Parkinson’s disease. It is possible that aggregates in the cell cause disease either by inhibiting cellular function, or by resulting in the death of the neurons. Regardless of how alpha synuclein aggregate effect the neuron, it is believed by many scientists studying Parkinson’s disease that the transmission of aggregated alpha synuclein enhances the disease. Current research for treatments of Parkinson’s disease focuses on reducing expression or aggregation of alpha synuclein protein and thereby protecting neural cells within the brain.

A team of researchers at Loyola University Chicago Stritch School of Medicine recently found that the movement of alpha synuclein to new cells appears similar to infection by viruses. Like many viruses, the alpha synucelin is taken into the cell and is held within a lysosome, a membrane bound sac that stores digestive enzymes. The lysosome keeps the digestive enzymes contained to prevent digestion of normal, healthy components in the cell. The normal function of the lysosome in the cell is breaking down food, damaged organelles, and potentially infectious agents. However, alpha synuclein is able to escape from the lysosome. This is similar to a method many viruses use to infect cells. Normally, when a virus escapes from a lysosome, it causes the release of the digestive enzymes that are stored within the lysosome. The enzymes are sensed as a toxin by the cell, and act as a signal to the cell that an infectious agent may be present. This causes the cell to begin a process called apoptosis, in which the cell dies to prevent the virus from being able to replicate.

While cell death during infection is beneficial to the host to prevent the spread of the infection, cell death in neurons can be very damaging to the host. Neurons are not able to regenerate efficiently, unlike most other cells in the body. As more neurons are infected by these alpha synuclein proteins, more neurons will be killed, causing more damage in the nervous system. In addition, neural cell death may also facilitate spread of alpha synuclein protein aggregates. The demonstration of alpha synuclein escaping from lysosomes has so far only been demonstrated in cell culture. The next step the research team wants to take is to determine if the alpha synuclein can escape from the lysosomes in animal models of Parkinson’s disease, and ultimately, in human patients with Parkinson’s disease. After it has been confirmed that alpha synuclein can indeed escape from lysosomes, the next step would be to determine if blocking this process could be used as a therapeutic to treat Parkinson’s disease. This research has the potential to lead to research more accurately describing the transfer of alpha synuclein aggregates from one neural cell to another. If this process is indeed responsible for the spread of Parkinson’s disease in the nervous system, then treatments could be developed to stop progression in the early stages of the disease.

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