Parkinson's Disease Research Paper

Parkinson’s Disease (PD) is named after James Parkinson, the individual responsible for discovering the condition in 1817 with the publication of his “An Essay on the Shaking Palsy”. Parkinson originally referred to this condition as “shaking palsy”, but overtime the condition became renamed. In general, PD is the neuronal degeneration in the part of the brain responsible for motor functions, particularly the substantia nigra (Valente 2004). Studies suggest that about 1.5 million people in the United States are affected by this nervous system disorder, with 50,000 cases arising annually. Males tend to be slightly more susceptibly to this condition than females. PD tends to begin around 60 and 70 years of age, but there have been cases seen

Lewy bodies are structures made of predominately proteins such as α-Synuclein and neurofilaments that form in the substantia nigra and other specific parts of the brain causing a loss in neurons, and therefore considered an indicator for neural disintegration. The neurons that Lewy bodies can be located on tend to be specific, but the distribution of such neurons containing the Lewy bodies is rather inclusive (Gibb 1988). Lewy bodies are extremely small (5-25 micrometers), intracytoplasmic, eosinophilic structures, meaning they are stained with eosin (a fluorescent acid) that then forms a salt when combined with an eosinophilic compound due to the positive and negative charge reaction. The goal of Gibb’s experiment was to determine whether there was an age-related relationship between the presence of Lewy bodies and Parkinson’s disease. After obtaining 273 brains, the nerve cells in the substantia nigra were examined and stained with eosin to force the fluorescence of Lewy bodies and make them visible. In conclusion, incidental Lewy body cases have the same progressive pathology as that seen in Parkinson's disease. Gibb also observed that Lewy bodies can be expressed in non-PD cases, acting as precursors to Parkinsonism (Gibb

These “cybrid” cell lines are a crucial step in the disease process and can be used to establish the extent of mitochondrial defects in PD. Cybrid’s are formed by placing mitochondria from a PD donor into a recipient who has no mitochondrial DNA present, supplying the donor’s mitochondria with a new genome. Now that the mitochondria is able to function based upon a different nuclear background, this technique is able to regulate whether the decrease in oxidation phosphorylation is directly correlated to the mitochondria. Swederlow used this same cybrid procedure and was able to determine that there were mitochondria deficiencies among the cell lines of PD patients, specifically in the mitochondrial complex I. These mitochondria also showed the production of free radicals, an uncharged molecule with an unpaired valence electron. Depending on the extent, free radicals can be very harmful to the cell, specifically damaging their membranes, proteins, and DNA. This damage is referred to as oxidative stress. An increase in free radicals gives rise to an increase in stress, which in turn intensifies the severity of Parkinsonism (Swederlow