Streaming Media

Type of Proposal

Digital Poster

Start Date

29-3-2016 1:00 PM

End Date

29-3-2016 2:20 PM

Faculty

Faculty of Science

Faculty Sponsor

Dr. Siyaram Pandey

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder often associated with memory impairment. According to the World Health Organization, approximately 48 million people worldwide live with the disease and this number is expected to triple by 2050. As AD is a poorly understood disease, there is currently no cure for the degeneration it causes. However, some studies have shown a possible correlation between Alzheimer’s disease and oxidative stress. Elevated reactive oxygen species are a result of inefficiency in the electron transport chain of the mitochondria, and can induce premature cellular senescence. The death of neurons can lead to the formation of neurofibrillary tangles and amyloid plaques, characteristic of the disease, in regions of the hippocampus and cerebral cortex. Due to the increasing prevalence of AD and the rapidly aging global population, a treatment that halts disease progression is absolutely necessary. It has been demonstrated that Ubisol-Q10 can stabilize the mitochondria and prevent neural loss by ultimately reducing the generation of free radicals. The neuroprotective properties of this water-soluble formulation of CoQ10 have been tested in a genetically predisposed transgenic mouse model expressing the human amyloid precursor protein and mutant human presenilin-1. Methylene blue has also been found to improve cognitive function in AD patients and reduce amyloid plaque levels, providing successful neuroprotection. Our objective is to use a combination of both Ubisol-Q10 and methylene blue to study how efficient this coalition of treatments is in postponing premature senescence in the same transgenic mice. The treatment will be accompanied by behaviour and biochemical studies along with ELISA and immunohistochemistry techniques to detect amyloid plaques, a marker of AD. This information will likely have a large impact on the field of neuroscience and the future of Alzheimer’s disease treatment.

Creative Commons License

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, 1:00 PM Mar 29th, 2:20 PM

Ubisol Q-10 in Combination with Methylene Blue as a Treatment for Alzheimer’s Disease in a Transgenic Mouse Model

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder often associated with memory impairment. According to the World Health Organization, approximately 48 million people worldwide live with the disease and this number is expected to triple by 2050. As AD is a poorly understood disease, there is currently no cure for the degeneration it causes. However, some studies have shown a possible correlation between Alzheimer’s disease and oxidative stress. Elevated reactive oxygen species are a result of inefficiency in the electron transport chain of the mitochondria, and can induce premature cellular senescence. The death of neurons can lead to the formation of neurofibrillary tangles and amyloid plaques, characteristic of the disease, in regions of the hippocampus and cerebral cortex. Due to the increasing prevalence of AD and the rapidly aging global population, a treatment that halts disease progression is absolutely necessary. It has been demonstrated that Ubisol-Q10 can stabilize the mitochondria and prevent neural loss by ultimately reducing the generation of free radicals. The neuroprotective properties of this water-soluble formulation of CoQ10 have been tested in a genetically predisposed transgenic mouse model expressing the human amyloid precursor protein and mutant human presenilin-1. Methylene blue has also been found to improve cognitive function in AD patients and reduce amyloid plaque levels, providing successful neuroprotection. Our objective is to use a combination of both Ubisol-Q10 and methylene blue to study how efficient this coalition of treatments is in postponing premature senescence in the same transgenic mice. The treatment will be accompanied by behaviour and biochemical studies along with ELISA and immunohistochemistry techniques to detect amyloid plaques, a marker of AD. This information will likely have a large impact on the field of neuroscience and the future of Alzheimer’s disease treatment.