Prize Winner

Best Research Talk

Streaming Media

Type of Proposal

Oral presentation

Start Date

29-3-2016 8:30 AM

End Date

29-3-2016 9:50 AM

Faculty

Faculty of Science

Faculty Sponsor

Dr. Siyaram Pandey

Abstract

As the most common neurodegenerative disorder, Alzheimer’s disease (AD) affects an estimated 46.8 million individuals worldwide. It is the primary cause of dementia and is associated with the deterioration of neural connections, which leads to neuronal death. AD manifests as memory and other cognitive deficits, impaired physical ability, and altered temperament. Its pathophysiology is not well understood, and so there have been no major breakthroughs in curing or slowing the progression of the disease. Research implicates oxidative stress as a possible mechanism in the development of neurodegeneration. Consequently, AD researchers have tested the strength of antioxidants such as oil-soluble coenzyme Q10 (CoQ10), in combating free-radical damage. Unfortunately, the low bioavailability of CoQ10 mandates effective doses well beyond FDA regulations. Nevertheless, our NRC collaborators synthesized a water-soluble formulation of CoQ10 known as Ubisol-Q10, which easily crosses the blood-brain barrier. In the past, our lab has tested neuroprotective capacities of this formulation in genetic and environmental toxin rat models of Parkinson’s disease, with positive results. Ubisol-Q10 was also assessed in vitro using fibroblasts from AD patients, where RT2PCR showed increased expression of autophagy genes (crucial in clearing cells of damaged structures). Now, we are extending this work to an in vivo mouse model of Alzheimer’s disease. Our transgenic mice expressed genes for human amyloid precursor protein and mutant human presenilin-1, predisposing them to develop early-onset AD. These mice were evaluated for 14 months, during which control groups received regular drinking water and treatment groups received water supplemented with Ubisol-Q10. ELISA tests for the treatment group showed a significant decrease in levels of circulating human amyloid beta, a key marker of AD. RT2PCR analyses to compare gene expression across groups are currently underway. Ultimately, we hope to understand the possible efficacy of Ubisol-Q10 in treating the encumbering illness that is Alzheimer’s disease.

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Creative Commons Attribution-Noncommercial 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

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Mar 29th, 8:30 AM Mar 29th, 9:50 AM

Evaluation of the Efficacy of Ubisol-Q10 Treatment in a Transgenic Mouse Model of Alzheimer's Disease

As the most common neurodegenerative disorder, Alzheimer’s disease (AD) affects an estimated 46.8 million individuals worldwide. It is the primary cause of dementia and is associated with the deterioration of neural connections, which leads to neuronal death. AD manifests as memory and other cognitive deficits, impaired physical ability, and altered temperament. Its pathophysiology is not well understood, and so there have been no major breakthroughs in curing or slowing the progression of the disease. Research implicates oxidative stress as a possible mechanism in the development of neurodegeneration. Consequently, AD researchers have tested the strength of antioxidants such as oil-soluble coenzyme Q10 (CoQ10), in combating free-radical damage. Unfortunately, the low bioavailability of CoQ10 mandates effective doses well beyond FDA regulations. Nevertheless, our NRC collaborators synthesized a water-soluble formulation of CoQ10 known as Ubisol-Q10, which easily crosses the blood-brain barrier. In the past, our lab has tested neuroprotective capacities of this formulation in genetic and environmental toxin rat models of Parkinson’s disease, with positive results. Ubisol-Q10 was also assessed in vitro using fibroblasts from AD patients, where RT2PCR showed increased expression of autophagy genes (crucial in clearing cells of damaged structures). Now, we are extending this work to an in vivo mouse model of Alzheimer’s disease. Our transgenic mice expressed genes for human amyloid precursor protein and mutant human presenilin-1, predisposing them to develop early-onset AD. These mice were evaluated for 14 months, during which control groups received regular drinking water and treatment groups received water supplemented with Ubisol-Q10. ELISA tests for the treatment group showed a significant decrease in levels of circulating human amyloid beta, a key marker of AD. RT2PCR analyses to compare gene expression across groups are currently underway. Ultimately, we hope to understand the possible efficacy of Ubisol-Q10 in treating the encumbering illness that is Alzheimer’s disease.