Modes of Action of Ubisol-Q10 Treatment in a Transgenic Mouse Model of Alzheimer's Disease
Type of Proposal
Oral presentation
Faculty
Faculty of Science
Faculty Sponsor
Dr. Siyaram Pandey
Proposal
As the most common neurodegenerative disorder, Alzheimer’s disease (AD) and other dementias affect an estimated 750 000 Canadians. AD is associated with the deterioration of synaptic connections in the brain, as well as widespread neuronal death. As its pathophysiology is not well understood, there have been no major breakthroughs in curing or slowing disease progression. However, research has implicated oxidative stress as a potential mechanism in the development of neurodegeneration. Consequently, the efficacy of antioxidants such as oil-soluble coenzyme Q10 (CoQ10), in combatting free-radical damage has been evaluated. In the past, our lab worked with a highly bioavailable, water-soluble formulation of CoQ10 known as Ubisol-Q10. The compound displayed strong neuroprotective capacities in genetic and environmental toxin rat models of Parkinson’s disease. Further, in vitro analyses of Ubisol-Q10 treatment using fibroblasts from AD patients have shown increased expression of autophagy genes (crucial in clearing damaged cellular structures). We extended this work to an in vivo transgenic rodent model, in which mice were predisposed to develop early-onset AD. During a 14-month incubation period, control groups received regular drinking water and treatment groups received water supplemented with Ubisol-Q10. Immunohistochemistry and biochemical analyses of neural tissue from the mouse groups, as well as behavioural studies validated the efficacy of Ubisol-Q10 treatment for AD. Now we aim to explore the modes of action of this formulation by evaluating autophagy levels, cell proliferation, and the response of supportive glial cells. Through investigating the mechanisms by which Ubisol-Q10 combats Alzheimer’s disease, we hope to further research towards the development of a treatment for this encumbering illness.
Modes of Action of Ubisol-Q10 Treatment in a Transgenic Mouse Model of Alzheimer's Disease
As the most common neurodegenerative disorder, Alzheimer’s disease (AD) and other dementias affect an estimated 750 000 Canadians. AD is associated with the deterioration of synaptic connections in the brain, as well as widespread neuronal death. As its pathophysiology is not well understood, there have been no major breakthroughs in curing or slowing disease progression. However, research has implicated oxidative stress as a potential mechanism in the development of neurodegeneration. Consequently, the efficacy of antioxidants such as oil-soluble coenzyme Q10 (CoQ10), in combatting free-radical damage has been evaluated. In the past, our lab worked with a highly bioavailable, water-soluble formulation of CoQ10 known as Ubisol-Q10. The compound displayed strong neuroprotective capacities in genetic and environmental toxin rat models of Parkinson’s disease. Further, in vitro analyses of Ubisol-Q10 treatment using fibroblasts from AD patients have shown increased expression of autophagy genes (crucial in clearing damaged cellular structures). We extended this work to an in vivo transgenic rodent model, in which mice were predisposed to develop early-onset AD. During a 14-month incubation period, control groups received regular drinking water and treatment groups received water supplemented with Ubisol-Q10. Immunohistochemistry and biochemical analyses of neural tissue from the mouse groups, as well as behavioural studies validated the efficacy of Ubisol-Q10 treatment for AD. Now we aim to explore the modes of action of this formulation by evaluating autophagy levels, cell proliferation, and the response of supportive glial cells. Through investigating the mechanisms by which Ubisol-Q10 combats Alzheimer’s disease, we hope to further research towards the development of a treatment for this encumbering illness.