Afflicting over one million Americans, Parkinson’s disease is one of the most devastating neuro-degenerative diseases in the world. A British physician, James Parkinson, first discovered this disease while observing people on the streets of London. He noted that certain individuals suffered from a tremor, which, along with muscle weakness, became worse with time. Even with standardized neurological examination by doctors today, Parkinson’s disease is still only detectible through careful observation of the patient. It was not until the late nineteenth century in which physicians finally began to understand the anatomy and physiology of Parkinson’s disease.

Throughout the past decade the knowledge base for Parkinson’s disease has increased tremendously. Parkinson’s disease has now been identified and cataloged by the medical community as a serious and potentially fatal neuro-degenerative disease. The disease’s symptoms, possible causes, mechanisms, and cures have been researched and studied by innumerable scientists and organizations.

Parkinson’s disease occurs when certain nerve cells, or neurons, in an area of the brain known as the substantia nigra die or bec

There are three specific groups of drugs used in controlling and reducing the effects of Parkinson’s disease: anticholinergic drugs, dopaminergic drugs, and dopamine-like drugs.

An additional study was conducted by a Japanese neurologist who found a form of L-dopa responsive “juvenile parkinsonism” (Yokochi, Narabayashi, Izuka, & Nagatsu 1984). Patients with this disorder had similar characteristics: disease onset before the age of 40 years, a positive family history, high incidence of foot dystonia, L-dopa-induced dyskinesias and motor fluctuations. Even with these differences it is still very similar to Parkinson’s disease. The axon deletion mutations in a gene on chromosome 6, named the “parkin” gene, have now been identified in a number of these families (Hatttori 1998). In recent studies, homozygous deletions and point mutations in the “parkin” gene have also been associated with early onset of Parkinsonism in European and North African families (Hattori 1998). Interestingly, these patients with parkin mutations do not have lewy bodies and also appear to have deficient parkin protein, whereas the concentrations of parkin is normal in Parkinson’s disease (Farrer et al., 2001). Even with the rarity of these cases, the genetic mutation discoveries have generated tremendous interest in the possibility that there may be additional genetic factors that cause Parkinson’s disease.

In identifying the cause of Parkinson’s disease as being either genetic or environmental (chemical) it seems that both of these factors contribute to and influence cell death, including additional unknown factors. The specific mechanism of cell death is still under research. However, there is a lot of supporting evidence that increased oxidative stress and free radical damage in the substantia nigra is related to cell death (Schapira 1999). This may be either a result of necrosis or apoptosis. Necrosis is the disruption and disposal of a cell and its organelles by phagocytosis through an inflammatory response (Schapira 1999). Apoptosis is characterized by DNA fragmentation, cell shrinkage, and a lack of inflammatory response. Also, mitochondrion is thought to have a very significant role in the events that lead to apoptotic cell death (Zamzami et al. 1997). There is now evidence that apoptotic cell death is present in the brain tissue of recently deceased Parkinson’s patients (Tatton et al. 1998).

A recent study by Lorene Nelson, PhD., a neuroepidemiologist at Stanford University School of Medicine, discovered that pesticide use and exposure in the home and garden increase the risk of developing Parkinson’s disease. Conducted with almost five hundred people who had newly been diagnosed with the disease, preliminary results reinforced what is already known about the increased risk of Parkinson’s disease associated with occupational exposure to pesticides. Researchers discovered that people who had been exposed to pesticides were about twice as likely to develop Parkinson’s disease than people not exposed to pesticides (Lazaroff 2000). Nelson stated, “Certain chemicals that an individual is exposed to in the environment may cause selective death of brain cells or neurons”. Nelson stressed that additional research needs to be conducted to determine why these neurons are being killed in certain circumstances.

Ninety-six patients were implanted with electrodes bilaterally in the subthalamic-nucleus group and thirty-eight patients were implanted in the globus-pallidus group. After three months the procedure was evaluated. It demonstrated that the stimulation of the subthalamic nucleus showed improvements in the motor control, over 49%. Also, the stimulation of the pars interna of the globus pallidus indicated an improvement of 37%. Statistical analysis of the last six months showed an even greater increase in mobility. Parkinson’s patients with subthalamic stimulation increased from

Some topics in this essay:
Galbin Jones, HC1 Benadryl, Cell Neurobiology, North African, School Medicine, James Parkinson, Rating Scale, Journal Medicine, Duvoisin Golbe, Hospital Bristol, parkinson’s disease, stem cells, et al, neural stem, neural stem cells, cell death, subthalamic nucleus, human neural, deep-brain stimulation, human neural stem, parkinson’s patients, human brain, patients parkinson’s disease, interna globus pallidus, et al 2001,