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Study Discovers New Contributor to Alzheimer’s Manifestation

Update Date: Apr 16, 2013 03:49 PM EDT
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The biological components and contributors to Alzheimer's disease have often been the subject of endless research as scientists hope to find a cure or better treatment for the neurodegenerative disease. Researchers have known for over 15 years that patients suffering from Alzheimer's develop two different types of brain lesions, with one possibly causing the other. It was not until this current study, done by David R. Borchelt, a professor of neuroscience, and Guilian Xu, an assistant research scientist from the University of Florida (UF) College of Medicine, that provided a clearer explanation as to why one lesion might be causing the development of the other.

The researchers used a mouse model to study these two lesions. Borchelt, who is also the director of the SantaFe HealthCare Alzheimer's Disease Research Center at UF and the McKnight Brain Institute, stated, "understanding how this sequence of events works is thought to be critical and could lead to new therapeutic approaches."

The researchers already knew that the lesion that develops first in Alzheimer's patients is an amyloid plaque, which is created by protein that has combined incorrectly with a small peptide, known as the amyloid-beta peptide. The second lesion was identified as the neurofibrillary tangle and tends to manifest in the later stages of the brain disease, when it has progressed drastically. By understanding how one lesion causes the other, scientists would ideally be able to find ways of preventing the sequence from happening, and ultimately stall the progression of the disease.

The researchers looked at cell functions and noted that all cells contribute to protein production. Since cells require a lot of energy to correctly manufacture protein, the researchers studied how certain proteins, like those found in the lesions, get folded incorrectly. They found that the presence of amyloid peptide that produces the plaque lesions also prevent cells from properly folding proteins. The fact that these cells cannot function like normal healthy cells might be the key in preventing the progression of the disease. If researchers can find a way to prevent the amyloid peptides from affecting cell function, Alzheimer's could be slowed down.

"This deficiency in cell function could set the stage for allowing the formation of the neurofibrillary tangles that seem to be the key pathology to symptoms," Borchelt stated. However, the research is still very early and more studies need to be done before confirming this direct link between cell functions and proteins.

The findings were published in the journal, Human Molecular Genetics.

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