Title

Ubisol-Q10 Treatment Prevents Substantial Memory Loss and Reduces β-Amyloid Plaques in a Transgenic Mouse Model of Alzheimer’s Disease

Prize Winner

Science

Streaming Media

Type of Proposal

Oral presentation

Start Date

29-3-2016 2:30 PM

End Date

29-3-2016 3:50 PM

Faculty

Faculty of Science

Faculty Sponsor

Dr. Pandey, Dr. Cohen

Abstract

There is currently no cure for Alzheimer’s disease (AD), a progressive, neurodegenerative disease that causes severe memory deficits and personal hardship. Animal models are useful for studying the progression of AD as neurodegeneration begins in the region of the brain called the hippocampus, which leads to changes in specific cognitive functions, such as spatial working memory. The Y-maze and novel object recognition (NOR) tests are frequently used in research to study working memory however, the novel location / novel object recognition (NL/NOR) test was developed more recently to study hippocampal-dependent spatial memory. When treated with water soluble coenzyme-Q10, calledubisol-Q10, cell cultures expressing human mutant presenilin-1 (PSEN1) show reduced levels of β-amyloid and protection against harmful reactive agents. This research suggested that ubisol-Q­10 may be an effective treatment for AD. The current study uses a double transgenic mouse model of AD expressing human mutant amyloid precursor protein (APP) and PSEN1 (1 – 1.5 year old male B6.Cg-Tg with APP/PSEN1) to investigate the effects of orally-administered ubisol-Q10 (fed 50 µg / mL in water supply starting at 1 month old) on tests of long-term memory and spatial working memory using modified Y-maze, NOR, and NL/NOR tests, compared to wild type mice (1 – 1.5 year old male C57BL/6J). Results using Repeated Measures ANOVA show that both wild type and ubisol-Q10 treated APP/PSEN1 mice perform better on tests of long-term memory and spatial memory compared to untreated APP/PSEN1 mice. The histopathological studies conducted after the behavioral tests confirm these results. Ubisol-Q10 treated APP/PSEN1 mice show remarkably low numbers of β-amyloid plaques in the hippocampus and cortex compared to untreated APP/PSEN1 mice. This study provides evidence to support the use of ubisol-Q­10 treatment in AD and further research should continue to investigate the cognitive and neurobiological effects of ubisol-Q10.

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Mar 29th, 2:30 PM Mar 29th, 3:50 PM

Ubisol-Q10 Treatment Prevents Substantial Memory Loss and Reduces β-Amyloid Plaques in a Transgenic Mouse Model of Alzheimer’s Disease

There is currently no cure for Alzheimer’s disease (AD), a progressive, neurodegenerative disease that causes severe memory deficits and personal hardship. Animal models are useful for studying the progression of AD as neurodegeneration begins in the region of the brain called the hippocampus, which leads to changes in specific cognitive functions, such as spatial working memory. The Y-maze and novel object recognition (NOR) tests are frequently used in research to study working memory however, the novel location / novel object recognition (NL/NOR) test was developed more recently to study hippocampal-dependent spatial memory. When treated with water soluble coenzyme-Q10, calledubisol-Q10, cell cultures expressing human mutant presenilin-1 (PSEN1) show reduced levels of β-amyloid and protection against harmful reactive agents. This research suggested that ubisol-Q­10 may be an effective treatment for AD. The current study uses a double transgenic mouse model of AD expressing human mutant amyloid precursor protein (APP) and PSEN1 (1 – 1.5 year old male B6.Cg-Tg with APP/PSEN1) to investigate the effects of orally-administered ubisol-Q10 (fed 50 µg / mL in water supply starting at 1 month old) on tests of long-term memory and spatial working memory using modified Y-maze, NOR, and NL/NOR tests, compared to wild type mice (1 – 1.5 year old male C57BL/6J). Results using Repeated Measures ANOVA show that both wild type and ubisol-Q10 treated APP/PSEN1 mice perform better on tests of long-term memory and spatial memory compared to untreated APP/PSEN1 mice. The histopathological studies conducted after the behavioral tests confirm these results. Ubisol-Q10 treated APP/PSEN1 mice show remarkably low numbers of β-amyloid plaques in the hippocampus and cortex compared to untreated APP/PSEN1 mice. This study provides evidence to support the use of ubisol-Q­10 treatment in AD and further research should continue to investigate the cognitive and neurobiological effects of ubisol-Q10.