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Published on: March 1, 2012
by Jeff Hansel for The Post Bulletin
Mayo Clinic scientists have shown that a tiny part of a cell might be at the root of Alzheimer’s disease development.
In a study published in PLoS One Thursday, Mayo neuroscientist Eugenia Trushina, biochemist Petras Dzeja and colleagues report that they determined mitochondrial organelles in the cells of mice became dysfunctional long before the transgenic mice displayed the dementia symptoms of Alzheimer’s.
“Even in embryonic neurons we can already see changes in mitochondria dynamics,” Trushina said.
High school biology teachers have long taught that mitochondria are the powerhouses of the cell. “They power everything in our body,” Trushina said, “so they basically are our little power plants. And when the power plant goes off, you know what’s happening — we do not have light. We do not have heat. We basically cannot sustain life.”
Mitochondria are especially needed by neurons, she said, that send messages in the brain. When a neural impulse travels from an axon (the tip of a nerve cell), mitochondria need to provide energy. If they’re dysfunctional, the axon can’t send its message.
“Mitochondrial dysfunction…is an underlying event in Alzheimer’s disease progression,” the PLoS One paper says.
The Mayo team now wants to know if the same thing they found in three strains of transgenic mice — ones genetically engineered to develop Alzheimer’s — is true in humans.
If it is, that could provide a target for early intervention. Stop the degradation of mitochondria, the researchers suggest, and perhaps Alzheimer’s could be delayed, or even prevented, from happening. The condition is the sixth-leading cause of death in humans, according to the Alzheimer’s Association.
They’re already preparing to study humans. That’s hard to do because people typically don’t go to a doctor for Alzheimer’s diagnosis until cognitive changes have already begun. That’s too late for the kind of research the Mayo team wants to do.
So the group is partnering with the Mayo Clinic Study of Aging at the clinic’s Alzheimer’s Disease Research Center in Rochester. “We have funding now from the National Institutes of Health that will allow us to test the changes,” Trushina said.
If the same holds true in humans as in mice, “then we can really now concentrate on dissecting the early mechanism of the dysfunction — and that will help to develop cure.” Information learned from mouse models does not always translate to use in humans.
But the Mayo researchers used a new field of science known as metabolomics (the study of metabolites). Instead of trying to find a single biomarker that might be associated with Alzheimer’s, researchers can study a more global picture of how biomarkers interact.
“We have, now, panels of biomarkers that we link to these early changes in mitochondrial dysfunction in these mice,” Trushina said. That offers potential targets for treatment. “We hope that we can prevent and repair the damage,” Trushina said.
With good mitochondria, she said, there’s good energy balance in the cell, good cell function and good memory. Without good mitochondria, “everything goes down.”
Trushina’s search for a cure is personal. “My mother-in-law is affected with Alzheimer’s disease. She’s 89 years old, and she’s a beautiful woman,” Trushina said. “And we certainly hope that we can help her and help a lot of people like her.”
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