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Research Grants 2006


To view an abstract, select an author from the vertical list on the left.

2006 Grant - Nichols

Amyloid-Beta Fibrils: A Trigger for the Innate Immune Response

Michael R. Nichols, Ph.D.
University of Missouri
St. Louis, Missouri

2006 New Investigator Research Grant

The innate immune system is an ancient self-defense mechanism for fighting off microbial invaders. Unlike the more specialized adaptive immune system, which takes time to mobilize immune cells and produce tailor-made anti-bodies to fight off specific foreign invaders, the innate immune system is a one-size-fits-all system that attacks any foreign matter in exactly the same manner. One of the key components of the innate immune system is the macrophage, an immune cell that can engulf and degrade foreign matter, particularly bacteria.

On their cell surface, macrophages display a set of proteins called toll-like receptors. Toll-like receptors typically react to molecules on the surface of bacteria, leading to an inflammatory response, but recent evidence indicates that the receptors may also be triggered by beta-amyloid, a small protein fragment that is a key suspect in Alzheimer's disease. Because inflammation may be an early event in Alzheimer's, activation of the toll-like receptors by beta-amyloid could be a major factor in Alzheimer pathology.

Michael Nichols, Ph.D., and colleagues plan to investigate the link between beta-amyloid and activation of toll-like receptors. He aims to identify which of the receptors may interact with which form of beta-amyloid. Because beta-amyloid molecules assemble themselves to form larger structures, not all forms of beta-amyloid may trigger the innate immune system.

The researchers also plan to investigate whether toll-like receptors on neurons can interact with beta-amyloid and whether such interactions influence neuronal survival. The work may lead to new insights into the toxicity of beta-amyloid, a facet of Alzheimer's disease that is still poorly understood.