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Poster Presentation: Young, Patel and Franklin

Poster Presentation: The effect of mitochondria-targeted antioxidant MitoQ on memory retention and neuropathology in aged 3xTg-AD mice

Melissa L. Young, Mital Patel and James L. Franklin
Department of Pharmaceutical and Biomedical Sciences, UGA College of Pharmacy

Story by Shelby Jarrett

Coal-fired generators pollute the air and nuclear power plants can melt down with catastrophic consequences. On a much smaller scale, the tiny powerhouses in every living cell, known as mitochondria, can also go haywire – churning out dangerous free radicals as well as life-giving energy.

When mitochondria produce highly reactive forms of oxygen, these rogue molecules put stress on all sorts of cells – contributing to degenerative diseases associated with aging.

“There’s a lot of research suggesting that oxidative stress is a major factor leading to the development of Alzheimer’s,” says Melissa Young, a Ph.D. student at UGA. “Malfunctioning mitochondria are probably the cause of this stress.”

She and her colleagues in the laboratory of neuroscientist James L. Franklin are looking for ways to interfere with oxidation. Like the rusting of a metal tool left outdoors for too long, exposure to certain species of oxygen in the body can weaken and damage cells. In the brain, this kind of oxidative stress can lead to the formation of plaques and tangles, abnormal structures that are the signature characteristics of Alzheimer’s during post-mortem examination.

Most people develop some plaques and tangles as they age, but people with Alzheimer’s develop lots more of these abnormal proteins, leading to loss of memory, thinking ability, and eventually basic bodily processes.

But what if an experimental drug could interfere? That is the question Young’s group has been exploring in 3xTg-AD mice, a special variety of mice bred to display three mutations associated with familial Alzheimer’s disease in humans. Like human Alzheimer’s patients, these animals lose memory and problem solving abilities at an accelerated pace as they age.

Young and her colleagues have been treating one group of these mice with an experimental mitochondria-targeted antioxidant compound called mitoquinone mesylate, or MitoQ. Those in the MitoQ group were better able to learn new behavioral cues and retain mental function than untreated mice, a promising finding given the absence of effective Alzheimer’s treatments.

“It could be another two or three years, or more, before any kind of specific antioxidant therapy drug could enter clinical trials in people,” says Young. “But we’re excited about it.”

Shelby Jarrett is a first-year graduate student in journalism at Grady College of Journalism and Mass Communication, UGA, and a reporter for Graduate Newsroom.