By Amy Norton
NEW YORK, Oct 11 (Reuters Health) -- In findings that could shed light on how Alzheimer's disease progresses, researchers have identified a common denominator in the three major types of brain cell damage associated with the disease.
Three proteins that normally exist in small amounts in brain cells are significantly more abundant in the damaged cells of Alzheimer's patients, according to researchers led by Dr. Jeffrey Kuret, an associate professor of medical biochemistry at Ohio State University in Columbus. While Kuret and his colleagues had previously found elevated levels of the proteins in two types of Alzheimer's-affected cells, their new research shows that the proteins are elevated in all three types of brain damage seen in the disease.
The findings are published in the October issue of the American Journal of Pathology.
The three types of Alzheimer's-related brain damage are known as plaques, tangles and granulovacuolar degeneration (GVD) bodies; the finding that a common molecular thread runs among them "adds another piece to the puzzle" of how Alzheimer's chips away at memory and comprehension, Kuret told Reuters Health.
Whether the proteins, which belong to a class known as casein kinase-1 (CK1) enzymes, cause or result from brain cell damage is unknown, Kuret said. Normally, the proteins help regulate activity within cells. "In Alzheimer's research," he noted, "we're starting at the end and working backward to disentangle this whole thing." Studying autopsied brain tissue from Alzheimer's patients, the researchers confirmed their earlier work that showed all three proteins dwelled in abundance in plaques and tangles.
Finding high levels of the proteins in GVD bodies was a "huge surprise," Kuret said. "This ties together the three types of lesions." When the researchers compared the Alzheimer's-damaged brain tissue to normal tissue samples, they found that the concentration of one of the CK1 proteins was 30 times higher in the diseased tissue; another was nine times higher and the third was more than twice as high.
"Now we have to ask, 'how does this 30-fold increase happen?'" Kuret added. "We want to get at the earliest stages."
If the CK1 proteins are found to actually damage brain cells, drugs may be developed to prevent this action, according to Kuret. If the protein elevation is just the body's response to brain damage, then it may serve as a chemical marker for Alzheimer's and aid in research and diagnosis of the disease.
