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Alzheimer's, other diseases, may benefit from first live studies of key cell structures

A new study describes for the first time a method of culturing important but poorly understood cell structures called Hirano bodies. The report by cellular biologists at the University of Georgia could shed light on numerous diseases in which Hirano bodies may play some role--including Alzheimer's disease, Lou Gehrig's Disease and cancer.

The research was published in the May issue of the Journal of Cell Science and was funded by the National Science Foundation (NSF) and the Alzheimer's Association.

Hirano bodies -- named for their discoverer -- have been known for several decades, and their presence in autopsy tissue of Alzheimer's patients has led to speculation that they may play a role in disease processes. Studying Hirano bodies, however, has been extremely difficult because they have been resistant to culturing in the laboratory.

The new study, led by cellular biologist Marcus Fechheimer, reports a novel way to create Hirano bodies in the lab, giving scientists their first tool to understand how the bodies may aid-or hinder--the progress of disease.

This is a wonderful example of why it is so important for scientists to pursue very basic, fundamental, curiosity-driven studies in cell biology, says Eve Barak, program director in NSFs division of cellular and molecular biosciences. Eventually such research will lead to something of great value to society.

Scientists have for three decades found Hirano bodies in the post-mortem examination of brain tissue from patients with neurodegenerative diseases, diabetes, alcoholism and cancer.

Understanding just what Hirano bodies do remains murky at best. They may change cells to make them more vulnerable to disease, but it's currently just as likely that they help battle disease; nobody knows. That's why the new results are exciting and offer a key tool for investigations of these structures.

The team used an unlikely candida
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Contact: Cheryl Dybas
cdybas@nsf.gov
703-292-8070
National Science Foundation
29-Apr-2002


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