Treatment

{Home} {Background Information} {Treatment} {Cutting Edge Treatment} {Genomic Analysis} {References}

Research Question: What role does the protein alpha-synuclein play in Parkinson's disease? __**Treatments:**__ To understand the treatments of this disease it is important to understand the chemical pathways in the brain that are affected and how they relate to the symptoms. First, the dopamine-secreting cells that succumb to apoptosis are located in the brain in a region called the substantia nigra, more specifically the pars compacta region of the substantial nigra (2). This region is in the center of the head behind the eyes and between the ears. The pars compacta region is indirectly responsible for motor function by releasing dopamine in response to stimuli. This dopamine is received by another area of the brain called the straitum. The straitum contains receptors for dopamine that in turn triggers neural synaptic functions that are mostly in control of movement (4). It is seen in Parkinson’s patients that upon diagnosis and onset of symptoms over 50% of the cells in the pars compacta have already died (6).

Often found of patients with Parkinson’s disease are the build up of Lewy bodies in the pars compacta as well as other areas of the brain. These Lewy bodies are a result of excess protein alpha-synuclein. These buildups in the brain have not been directly attributed to cell death but are known to cause problems in other areas of the brain with other diseases such as dementia (2).

There is no cure of Parkinson’s disease. There is especially to way to reverse the negative impact on the brain. The current method for treating Parkinson’s disease is a combination of Levodopa (L-dopa), which converts to dopamine in the brain, and some type of dopamine receptor enhancer drug (5). These drugs are usually paired with some type of antidepressant to increase quality of life. The increased levels of dopamine in the brain temporarily enhance the motor functions of the patient. The down side of Levodopa is that it must be given in high quantities to travel through the blood brain barrier to get to the pars compacta. The high quantity in the body results in involuntary movements and stiffness (2).

It has been observed that up to 15% of Parkinson’s disease cases may be hereditably linked. Since the cell death in the pars compacta region is random, there seems to be no visible reason why this may be. If it is also known that a build up of Lewy bodies in other areas of the brain are known to cause other diseases such as dementia, and the same Lewy bodies are also found in the pars compacta region of the brain, then it could be possible that these Lewy bodies are resulting in negative effects in the pars compacta area of the brain (2).

Alpha-synuclein is the primary protein that causes the formation of these Lewy bodies. Its function in the brain is a soluble membrane interacting protein that may serve in preliminary synaptic functions (9). It has been found that several types of the alpha-synuclein protein exist in Parkinson’s disease patients because of mutations. These mutations cause the formation of fibers on the protein, which may be a reason when they are more likely to form Lewy bodies (9). Since the negative effects of these mutations happen after reproductive years, the mutations are passed on to the next generation.

{Home} {Background Information} {Treatment} {Cutting Edge Treatment} {Genomic Analysis} {References}