Ubsiol-Q10 as a Treatment for Alzheimer's Disease in a Transgenic Mouse Model
Type of Proposal
Oral presentation
Faculty
Faculty of Science
Faculty Sponsor
Siyaram Pandey
Proposal
Alzheimer’s disease (AD) is a progressive, fatal neurodegenerative disease affecting over 500 000 Canadians and is caused by death of neurons, formation of amyloid plaques, and impairments in memory and behaviour. Currently there is no treatment available for AD and with increases in the aging population this will result in exponential growth in socioeconomic and healthcare cost. Hence, it is urgent to identify remedies to halt the progression of AD. A water-soluble formulation of Coenzyme Q10 (Ubisol-Q10) has shown to provide neuroprotection in animal models of Parkinson’s disease. We investigated if this formulation can halt the progression of AD in a genetically predisposed double transgenic mouse model of AD. These transgenic mice express the human amyloid precursor protein and the mutant human presenilin 1. The transgenic mice were divided into two groups; one receiving Ubisol-Q10-supplemented water and the other regular water. In addition, there was a wild-type group acting as a control. The treatment continued for one year and four months following which the mice were sacrificed and immunohistochemistry was conducted to measure the levels of neurodegeneration and astrocyte activation. Immunohistochemistry and Congo red fluorescence both showed a decrease in the level of amyloid plaque in the hippocampus of Ubisol-Q10 treated mice compared to the untreated groups. GFAP immunohistochemistry staining showed increased astrocyte activation in the hippocampus and cortical regions of the treatment group compared to the untreated group. Thus, Ubisol-Q10 has demonstrated potential in providing neuroprotection against neurodegenerative diseases like AD.
Start Date
29-3-2016 8:30 AM
End Date
29-3-2016 9:50 AM
Ubsiol-Q10 as a Treatment for Alzheimer's Disease in a Transgenic Mouse Model
Alzheimer’s disease (AD) is a progressive, fatal neurodegenerative disease affecting over 500 000 Canadians and is caused by death of neurons, formation of amyloid plaques, and impairments in memory and behaviour. Currently there is no treatment available for AD and with increases in the aging population this will result in exponential growth in socioeconomic and healthcare cost. Hence, it is urgent to identify remedies to halt the progression of AD. A water-soluble formulation of Coenzyme Q10 (Ubisol-Q10) has shown to provide neuroprotection in animal models of Parkinson’s disease. We investigated if this formulation can halt the progression of AD in a genetically predisposed double transgenic mouse model of AD. These transgenic mice express the human amyloid precursor protein and the mutant human presenilin 1. The transgenic mice were divided into two groups; one receiving Ubisol-Q10-supplemented water and the other regular water. In addition, there was a wild-type group acting as a control. The treatment continued for one year and four months following which the mice were sacrificed and immunohistochemistry was conducted to measure the levels of neurodegeneration and astrocyte activation. Immunohistochemistry and Congo red fluorescence both showed a decrease in the level of amyloid plaque in the hippocampus of Ubisol-Q10 treated mice compared to the untreated groups. GFAP immunohistochemistry staining showed increased astrocyte activation in the hippocampus and cortical regions of the treatment group compared to the untreated group. Thus, Ubisol-Q10 has demonstrated potential in providing neuroprotection against neurodegenerative diseases like AD.