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For mitochondria, bigger may not be better
Date:8/23/2012

tochondria," said DuBoff. "This mitochondrial dynamic happens continuously in almost all cells. Interruption of this process leads to cell death, and loss of nerve cells in the brain results in loss of functionmemory loss and difficulty in comprehension and coordination." The presence of defective tau, then, interrupts the functioning of mitochondria and contributes to neurodegeneration.

To further observe how mitochondrial dynamics were affected by the presence of defective tau, the researchers modified two sets of genes in human-tau-expressing flies, one that controls how mitochondria divide and another that guides how they come together. When the expression of the gene that causes mitochondrial lengthening, or fusion, was increased, the level of neurodegeneration in the flies increased and the flies were sicker. Conversely, when the expression of the gene that causes mitochondrial division, or fission, was increased, the defect reversed and the flies' condition improved.

The study also showed that, in addition to tau, two other key proteins influenced the neurodegenerative process: DRP1, which helps in the fission of mitochondria, and actin, which is essential to maintaining cell structure and movement. A previous study in Feany's lab had shown that the presence of defective tau hampers the activity of actin. With this knowledge, the researchers were able to piece together the relationship among the three proteins. DRP1 and actin are interdependent: the regulatory state of actin is essential for DRP1 and mitochondria to come together, thus preserving mitochondrial dynamics. But the presence of defective tau harms this relationship, rendering DRP1 incapable of maintaining mitochondrial dynamics, which ultimately leads to neurodegeneration.

"We have a good idea now of where the process starts. We know it ends with neurodegeneration, and with this study, we know some milestones along the way," said Feany. "But we still have to fill in th
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Contact: David Cameron
david_cameron@hms.harvard.edu
617-432-0441
Harvard Medical School
Source:Eurekalert

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