Previous studies have indicated the role of immune system in Alzheimer’s disease (AD), but now, a group of researchers at the University of California, Irvine, has indicated that certain unexpected parts of the immune system may have an increased role in the development of this disease. The study, titled “The adaptive immune system restrains Alzheimer’s disease pathogenesis by modulating microglial function,” was published in the journal Proceedings of the National Academy of Sciences in February, 2016.
The objective of the research was to examine if adaptive immune system has any role to play in AD pathogenesis. For the purpose of the research, scientists bred genetically modified Alzheimer’s disease mice. The mice used for the experiment lacked three different immune cell types – T-cells, B-cells, and NK-cells – due to genetic adjustments. Subsequent observation at the end of six months revealed that the brains of mice bereft of the three different immune cell types had two times beta-amyloid accumulation when compared with mice suffering from AD with untouched immune systems.
Dr. Mathew Blurton-Jones, assistant professor of neurobiology and behavior at the University of California, Irvine, said, “We were very surprised by the magnitude of this effect. We expected the influence of the deficient immune system on Alzheimer’s pathology to be much more subtle.”
The researchers’ next course of action involved understanding as to what triggered increase in levels of beta-amyloid in the genetically transformed rats, despite the loss of T-cells, B-cells and NK-cells. For this, scientists analyzed the interactions between these cells and microglia in the brain. To this, Samuel Marsh, doctoral student at the Department of Neurobiology and Behavior, University of California, Irvine, explained, “We found that in Alzheimer’ mice with intact immune systems, antibodies – which are made by B-cells – accumulated in the brain and associated with microglia. This, in turn, helped increase the clearance of beta-amyloid.”
The researchers then replaced the immune cells to check for reverse beta-amyloid buildup by transplanting healthy bone marrow stem cells into the immune-deficient AD mice, which would lead to a reconstitution of the missing T-cells, B-cells and NK-cells. It was found that on replacement of the immune cells, the B-cells could then once again produce antibodies that reached the brain and aided microglia in eliminating beta-amyloid.
The researchers wrote, “Our study therefore adds to a growing area of research that highlights the importance of the peripheral immune system in CNS function and Alzheimer’s disease, and demonstrates the need to better understand how these peripheral cell populations act in concert with microglia to influence the CNS in both normal and diseased conditions.”
As the immune system becomes weaker with growing age, Dr. Blurton-Jones said, “We know that the immune system changes with age and becomes less capable of making T- and B-cells. So whether aging of the immune system in humans might contribute to the development of Alzheimer’s is the next big question we want to ask.”
Significance of study
The research indicates that the alterations in peripheral immune function owing to age, co-occurring disorders or genetic variations might be the factors triggering the development and advancement of AD in old people. This is important as the Alzheimer’s Association statistics reveal that approximately one in nine Americans is suffering from the disease. Also, an estimated 5.3 million people in the U.S. were affected by AD in 2015. And it is the sixth leading cause of deaths in the country.
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