Microglial Acivation as a Possible Mechanism for Neuroprotection by CoQ10

Submitter and Co-author information

Joseph C. Correia, University of WindsorFollow

Type of Proposal

Oral presentation

Streaming Media

Faculty

Faculty of Science

Faculty Sponsor

Dr. Pandey

Start Date

24-3-2015 1:00 PM

End Date

24-3-2015 1:50 PM

Importance of the Project

Parkinson’s disease is a neurological disorder that affects 100,000 people across Canada with 5,500 new cases diagnosed each year. While commonly considered a disease for the elderly, approximately 40% of people diagnosed are under the age of 60 according to the Parkinson’s Society of British Columbia. Parkinson’s disease is characterized by loss of motor control seen as tremors, dyskinesia, loss of balance and muscle rigidity. As the disease progresses, cognitive and behavioral defects can also be experienced. While this disease has a substantial impact on Canada and the worldwide population, there is still no cure. This research aims to find a possible treatment for this widespread disease enabling the progression of Parkinson’s disease to be prevented.

Existing State of Knowledge

One of the most commonly used treatment options is the administration of levodopa. This is a natural compound found in the human body that acts as precursor to the neurotransmitter dopamine. The depletion of this neurotransmitter is responsible for the onset of Parkinson’s disease as discovered by Ehringer and his team of researchers. Levodopa is able cross the blood-brain barrier and temporarily restore levels of dopamine thereby causing a partial relief from the loss of motor control. The reduction in dopamine is primarily due to the death of dopaminergic neurons in the substantia nigra located in the midbrain. Since oxidative stress is thought to be one of the primary mechanisms driving this degeneration, it was thought that an antioxidant could be used as an effective treatment. One such antioxidant is coenzyme Q10 (CoQ10). This compound is an electron transporter present in the mitochondria. Previous studies have used an oil-soluble formulation of this compound, but the dosage required to induce neuroprotection was too high for practical purposes. However, the water-soluble formulation of CoQ10 has been shown to protect the dopaminergic neurons from degeneration while maintaining a practical dosage. The mechanism behind this is still yet to be discovered and is the main goal of this research.

Research Question

Does the water-soluble formulation of CoQ10 induce microglial activation to prevent neurodegeneration by secreting neurotropic factors such as BDNF and GDNF?

Methodology

Rats will be used as the model organism to conduct this study. Paraquat, a potent neurotoxin shown to damage dopaminergic neurons of the substantia nigra, will be used for the model. These rats will be divided into three treatment groups. One group will receive therapeutic treatment by being injected with paraquat and subsequently be treated with CoQ10. The second group will receive paraquat injections without CoQ10 treatment. The last group will only receive saline injections and will serve as a control group. The levels of BDNF and GDNF in these three groups will be compared using immunohistochemistry.

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Mar 24th, 1:00 PM Mar 24th, 1:50 PM

Microglial Acivation as a Possible Mechanism for Neuroprotection by CoQ10