Parkinsons Disease Research

Animal Cell Models

The aim of Parkinson’s research using animal cell models is twofold. Firstly, animal cell models help researcher gain a better understanding of the pathology and molecular controls governing Parkinson’s disease. Secondly, it allows researchers to trial potential treatments and therapies for this currently incurable disease.

Another important aspect of animal cell model research is the identification of factors that may protect the dopamine-producing neurons from decay, thus slowing down or ultimately, preventing cell death.

Research into Apoptosis (Cell Death)

In healthy people, cells are genetically “programmed” to die naturally as a part of normal development. This process, known as apoptosis, is a natural process of programmed cell death. Current Parkinson’s research indicates that this naturally occurring cellular process, responsible for preventing disease, becomes dysfunctional in patients with Parkinson’s disease.

Reactive Oxygen Species (ROS)

Reactive oxygen species (ROS) is a term used to describe any free radical where oxygen is involved. ROS are produced as part of the process of cellular metabolism. Overproduction of ROS causes a state of oxidative stress where the body simply cannot cope with the onslaught of excess free radicals. This, in turn, may trigger the onset of Parkinson’s disease.

Recent Parkinson’s research has also shown that mitochondrial dysfunction in the brain of PD patients, speeds up the production of ROS, thus accelerating dopaminergic neural cell death.

Fascinating research into the aging process and its impact on the development of PD has revealed that very elderly people are not necessarily predisposed to Parkinson’s disease. It would appear that aging, in itself, does not reduce the number of dopamine-producing neurons in the brain, rather the increased oxidative stress placed upon the neurotransmitters, during the protracted aging process, actually triggers dopaminergic cell death in the brains of elderly people.

Stem Cell Research and Parkinson’s Disease

Pioneering stem cell research has recently established the presence of stem cells in adult brains. These findings have huge implications for developing an effective treatment for PD, whereby adult stem cells can be stimulated to become dopaminergic neuron transmitters.

Transplantation Therapy: Results, to date, are encouraging that eventually stem-cell-based regenerative transplantation therapies will become available for treating patients with Parkinson’s disease. Trials are ongoing to refine the process of replacing dying dopaminergic neurons in patients suffering from Parkinson’s disease, using transplantation therapy.

Experiments have already confirmed that large concentrations of embryonic stem cells can be cultured successfully under laboratory conditions. The problem lies with the cell culture of adult neuronal stem cells, which are seldom found in adult cell tissue or, where present, are rarely found in sufficient numbers for viable transplantation therapy.

Large concentrations of stem cells are required for successful stem cell replacement therapies. The dilemma facing Parkinson’s researchers is whether to use grafted embryonal stem cells, which are present in abundance, or to concentrate on developing the adult patient’s own cells, when available, for stimulating the activity of dopamine-producing neurons. Using the patient’s own stem cells has the distinct advantage of overcoming cell rejection. Although in the early stages, Parkinson’s research is ongoing into the application of adult stem cell transplantation therapy.

Exercise to Reduce the Risk of Parkinson’s Disease

A number of recent studies have shown that forced exercise can improve motor function in animal cell models. Exercise may also help protect the brain cells affected by Parkinson’s disease.

One such study conducted at the University of Pittsburgh and presented to the Annual Meeting of the Society for Neuroscience, San Diego (October 2004) concluded that exercise may help prevent degeneration of the dopamine cells associated with the onset of Parkinson’s disease.

One possible explanation of the exercise theory, according to Michael J. Zigmond, Professor of Neurology, Neurobiology and Psychiatry, and Co-director of the Parkinson’s Disease Center of Excellence, University of Pittsburgh School of Medicine, is the fact that “exercise stimulates production of key proteins that are important for the survival of neurons.”

A similar Parkinson’s research project headed by Annie D. Cohen at the Center for Neuroscience, University of Pittsburgh School of Medicine, demonstrated that fewer dopaminergic neurons died in the brains of rats forced to exercise their limbs for a seven-day period before being induced with Parkinson’s disease. The control group consisted of rats that had not been forced to exercise before receiving the toxin. In this particular experiment, the brain tissue of both the rats forced to exercise and the control models was analyzed 28 days following injection with 6-OHDA. The results revealed that six percent of dopaminergic neurons had died in the rats forced to exercise before being injected with 6-OHDA. The rats that had not been forced to exercise before receiving the toxin showed an 87 percent reduction in dopaminergic neurons.

Findings from this study also demonstrated the protective effect produced by exercise against dopamine neuron cell degeneration. “Our data,” explains Cohen, “suggest the possibility that exercise can make dopamine neurons resistant to neurotoxins and may therefore be a useful therapy for Parkinson’s disease.”

Encouraged by the possibility that forced exercise might be a major factor in protecting against the development of PD, several Parkinson’s researchers are currently focusing on the implications of controlled and regular exercise programs on patients with PD.


Freed, C.R., Greene, P.E., Breeze, R.E., Tsai, W-Y., DuMouchel, W., Kao, R., Dillon, S., et al. (2001, March 8). Transplantation of embryonic dopamine neurons for severe Parkinson’s disease. New England Journal of Medicine 344(10), 710-719.

National Institutes of Health (2004). Stem cell basics.

Starkov, A., Fiskum G. (2002, November). Generation of reactive oxygen species by brain mitochondria mediated by alpha-ketoglutarate dehydrogenase [Program No. 194.17]. Society for Neuroscience Annual Meeting Abstracts.

Thannickal, V.J., Fanburg B.L. (2000, December). Reactive oxygen species in cell signaling. American Journal of Physiology – Lung Cellular and Molecular Physiology 276(6), L1005-1028.

University of Pittsburgh Medical Center. (2004, October 24). Exercising limbs protects brain cells affected by Parkinson’s, University of Pittsburgh researchers report in small animal studies at Society of Neuroscience meeting. UPMC Press Release.