Nov 14, 2006

Biology prof publishes Alzheimer's article

by Joanne Tang, News Editor

The human mind is a tricky thing — it is immensely complex, full of intricacies that have made scientists wonder and explore its depths for centuries. Unfortunately, one thing scientists have noticed is that sometimes, the brain fails to archive all the memories and facts humans accumulate over the years. For the last 100 years, scientists have, piece by piece, made progress in putting together the puzzle that is Alzheimer’s disease.

Here at Liberty, Dr. David DeWitt, professor of biology, has published his piece of the puzzle.

He and a colleague from the University of Virginia set out to research and experiment in the field of Alzheimer’s disease. At the start of their collaboration in 1999, their funding came from another grant.

“(The grant) allowed us to do the ground work,” DeWitt said.

When the National Institutes of Health gave DeWitt a four-year $122,000 grant, DeWitt was able to purchase a $40,000 fluorescent microscope and a bio-imaging machine that detects protein levels in samples and compares them. With the equipment, he was also able to do research at Liberty rather than drive to Charlottesville to conduct his experiments. He said it was helpful, especially when he had experiments that required more than a day.

The project initially began in a different direction. DeWitt was examining cell death, but as research progressed, DeWitt saw that the problem had more to do with cell transport. The research team then took off in this new direction.

This avenue was directly related to synapse loss, one of the hallmarks of Alzheimer’s disease. Synapse loss disrupts the transport of mitochondria, which provides energy to the cells.

If you (look at) spinal nerves, it has the main part of the cell in the spine but it has synapses far away,” DeWitt said.

He explained that the connection between the nerves and the axons in the brain are disrupted and this may be one of the causes of synapse loss.

The premise of the resulting article, “Peri-nuclear clustering of mitochondria is triggered during aluminum maltolate induced apoptosis,” is that failure transport mitochondria leads to synapse loss because mitochondria are not there to provide the energy the synapse needs. He said the defect might be the “inability to send mitochondria where it needs to be.”              

“My focus had been to understand the fundamental triggers that lead to Alzheimer’s pathology,” he said. He said the research into Alzheimer’s pathology starts at the bottom. “If we don’t know the central problem, we don’t know how to fix it.”

Another benefit of being able to experiment at Liberty was that DeWitt could involve students. Three of the contributors to the article are Liberty students. Senior Brigette Townsend has been working on the project since her freshman year. Kathleen Griffioen graduated from Liberty and is a graduate student at George Washington University.

“My experience here has taught me important lab techniques and principles and has been a great introduction and foundation for a research career,” said Townsend.

The work that DeWitt and his colleagues have done so far has contributed to the university in a magnitude of ways. One is that students in his biology classes are conducting experiments that are related to the Alzheimer’s work that DeWitt and his colleagues have done.

“Students have access to the research materials I had,” said DeWitt. He said this allowed students to be on a level field with other universities.

DeWitt is currently working on obtaining a grant from Wake Forest University.

There are still many mysteries and questions that have yet to be answered. With the research being conducted and the minds hard at work at unraveling the way this degenerative disease works, every day of progress is one step closer to helping those with Alzheimer’s disease.

Contact Joanne Tang at jtang@liberty.edu.

 


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