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How a Slime Mold
Came to the Aid of
Alzheimer's Research

by Kathleen Cason

EMAIL THIS     PRINTABLE VERSION

Intro/Proteins run amuck  |  The path to hirano bodies
Serendipity and beyond
  |   What's ahead

Life of Slime

What Goes Wrong
in Alzheimer's Disease

 


Blue shading indicates affected regions of the brain at various stages of Alzheimerís disease: preclinical (top), mild or moderate (middle) and severe symptoms (bottom).

(Top) Ten to 20 years before any indication of Alzheimerís disease is evident, the brainís memory centers begin to shrink.

(Middle) As the damage spreads, an otherwise healthy person experiences impaired memory, language and thinking.

(Bottom) During the final stages of Alzheimerís disease, brain atrophy is widespread and patients no longer recognize loved ones nor have the ability to communicate.

For more information about Alzheimerís disease, log on to www.alzheimers.org

Intro

In an ancient Persian fable, three princes from the kingdom of Serendip go out into the world to gain experience. During their adventures, they find they have a gift for making unexpected discoveries.

Like those fabled princes, UGA cell biologist Marcus Fechheimer and his research team have discovered they too have a gift for serendipity.

In the course of trying to understand how proteins “know” where to go in a cell, the researchers unexpectedly stumbled upon an unusual cellular structure normally associated with Alzheimer’s and other neurodegenerative diseases.


“I didn’t think we were working on anything that had to do with Alzheimer’s disease,” said Fechheimer, who uses a slime mold as his lab’s version of a “guinea pig.”

“We didn’t expect to find a structure in a slime mold that is present in increased amounts in people with Alzheimer’s — particularly present in the brain’s major site of learning and memory. That’s where these things accumulate,” he said.

Fechheimer’s team not only chanced upon this unusual structure — called a Hirano body — in a slime mold but also figured out how to force cells to produce them on command in the laboratory. Up till now, these structures could only be studied in brain tissue of people who had died. Because of this discovery, scientists will be able to study Hirano bodies in living cells for the first time and unravel the mysteries of this little-understood protein deposit.

Though Hirano bodies are common in the brains of people diagnosed with dementia, their role in disease, if any, is unclear.

“We don’t know if a Hirano body is good or bad or why it’s there or how it forms,” said Ruth Furukawa, a UGA research scientist who co-directs the study.

Proteins run amuck

What causes neurodegenerative diseases like Alzheimer’s is still largely unknown, but something destroys nerve cells in the brain over a period of time as victims gradually lose their minds.

In the hunt for cause and cure, scientists have focused on various abnormal protein deposits that mar diseased brains. Deposits called plaques and tangles have captured the most attention. Hirano bodies, while not at the forefront of Alzheimer’s research, are another type of protein deposit associated with the disease.

“Hirano bodies are certainly more prevalent in brains from patients who are suffering from dementias, probably any type,” said James Bamburg, one of Fechheimer’s collaborators and a professor of biochemistry and molecular biology at Colorado State University. “Hirano bodies also occur in brains of individuals with normal cognitive function but usually increase in number with age.”

Nearly four decades have passed since Asao Hirano, an eminent neuropathologist at Montefiore Medical Center in New York, first discovered the peculiar deposit in the brain’s memory center. Since then Hirano bodies have been reported in the brains of people with neurodegenerative diseases, as well as diabetes, stroke and alcoholism.

“Making a Hirano body may be a cellular mechanism for dealing with run-amuck proteins,” said Furukawa, who manages the day-to-day operation of the lab. “That’s just a hypothesis.”

Run-amuck proteins certainly seem to play some role in all the diseases where Hirano bodies are found.

“Perhaps Hirano bodies do nothing; perhaps they’re part of cell death; or perhaps they are adaptations to stress that are good for cells,” Fechheimer said. “Because they’re seen in so many diseases, it’s worth finding out.”

After more than 20 years probing basic questions in cell biology, Fechheimer’s team is well positioned to explore the role of Hirano bodies in cells and in human disease.

NEXT

Intro/Proteins run amuck  |  The path to hirano bodies 
Serendipity and beyond  |  What's ahead
 

EMAIL THIS     PRINTABLE VERSION


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