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2016 Grants - Colton
Onset of Immune Pathology in Alzheimer’s Disease
Carol A. Colton, Ph.D.
Duke University Medical Center
Durham, North Carolina
2016 Zenith Fellows Award
How is the immune system and inflammation involved in Alzheimer’s disease?
The brain contains specialized cells known as microglia, which function as part of the immune system. Like other parts of the immune system, the activity of microglia is controlled by complex networks of cells and molecules. Such control is essential, since the microglia can cause damage to healthy nerve cells when they are overactive. But if they are underactive, microglia may fail to protect the brain from infections or disease.
It is commonly observed that people who have Alzheimer’s disease have high levels of inflammation in the brain, presumably caused by the immune system. Such inflammation may be a response to the disease process, but it may also increase brain damage if it becomes excessive. Scientists do not fully understand the role of inflammation or the immune system in Alzheimer’s disease.
Carol A. Colton, Ph.D. and colleagues have discovered a protein, known as RNAseT2, which reduces the activity of the immune system in the brains of mice that have an Alzheimer’s-like condition. They suspect that RNAseT2 is released by nerve cells that are being stressed by the immune system in an attempt to tell microglial cells to suppress their activity. Such an effect may initially help to preserve nerve cell function, but can have negative effects if it goes on for too long. The researchers hypothesize the dysregulation of this process may contribute to brain damage in Alzheimer’s disease. For the current studies, the research team will study how this protein affects the activity of microglial cells growing in laboratory dishes. They will also measure levels of RNAaseT2 in brain tissue from people at different stages of Alzheimer’s disease to determine how this relates to disease progression.
The research to be conducted by Dr. Colton’s team will provide new insights into the role of the immune system and inflammation in Alzheimer’s disease. It may also suggest strategies for the development of novel treatments that regulate the immune system in Alzheimer’s disease, possibly slowing or halting disease progression.