By Sonal Gagrani

The Federation of American Societies for Experimental Biology (FASEB) brought together neuroimmunologists from all over the world to Big Sky, Montana in July to discuss their current and upcoming research on mechanisms and therapeutics in neuroimmunology.

They covered a plethora of topics in the field from multiple sclerosis, a neurodegenerative brain disorder, to neuroprotection by microglia, the resident immune cells of the brain, to the effects that intestinal imbalances can have on the brain via the blood brain barrier.

My primary focus at the meeting was to expand my knowledge on Alzheimer’s disease (AD), a dementia-causing neurodegenerative disease of the central nervous system that I am currently researching.


Lauren Kane with her poster at the FASEB conference

We were fortunate to have Lauren Kane, a rising senior in Dr. Carol Colton’s lab at Duke and the only undergraduate student with a poster at the conference, be able to present her work on her Alzheimer’s mouse model.

It is known as a CVN-AD model and has many pathologies found in AD such as β-amyloid plaque formation, neuron loss, tau protein defects, and behavioral deficits. Lauren is studying the changes in myelin, the primary make-up of white matter in the brain. Myelin wraps around axons in order to allow faster communication between neurons. She has found that there is some breakdown in myelin in the CVN-AD model, and this could lead us to find treatments for AD that promote remyelination in the brain.

Matthew Kan, an MD/PhD student in Dr. Michael Gunn’s lab at Duke, also presented his work on Alzheimer’s at the conference. He showed in the CVN-AD mouse model that a possible mechanism of neuronal death may be decreased arginine, an essential amino acid in the brain. Microglia produce arginase-1, an enzyme that breaks down arginine, and Matthew found that blocking arginase-1 activity reversed some neurodegeneration found in the CVN-AD mice. This arginine depletion pathway is known to suppress the brain’s immune system rather than cause inflammation, which many people thought was the mechanism for AD pathology in the past. These results may shift some focus to arginine in looking for AD treatments.

The conference strived to integrate and improve neuroimmunology research by providing a venue for creating connections with the experts in the field. There are many therapeutics for brain disorders in progress that key in on the importance of the brain’s immune system in regulating pathology.