Lupus Research Alliance Announces Awards of up To $1 Million to Uncover Root Causes of Lupus

NEW YORK, Nov. 9, 2017 /PRNewswire-USNewswire/ -- The Lupus Research Alliance is proud to announce the 2017 recipients of the Dr. William E. Paul Distinguished Innovator Awards in Lupus and Autoimmunity. Michael Carroll, PhD, Children's Hospital Boston, is studying why and how lupus attacks the brain and central nervous system (CNS). John D. Mountz, MD, PhD, The University of Alabama at Birmingham, is investigating a new explanation for how lupus develops and the reason some people are at greater risk for flares and kidney disease. Both projects have the potential to stimulate innovative strategies for prevention, treatment, and cure of lupus.

Lost Connections Between Nerves May Cause CNS Lupus                                               

CNS lupus refers to neuropsychiatric issues experienced by many people with lupus, including headaches, confusion, depression, and memory and vision problems as well as seizures, strokes or changes in behavior. Dr. Carroll discovered a link between CNS lupus and a loss of "synapses"—or the connections between nerves that allow the flow of information in the brain, much like bridges allow cars to pass from one stretch of roadway to the next. Importantly, the synapse bridges that are destroyed in lupus are in a specific area of the brain that controls behavior.

A major breakthrough for understanding CNS lupus, Dr. Carroll found that an antibody that blocks interferon, a key molecule of the immune system, could prevent CNS lupus by defending these synapses from attack. With his Distinguished Innovator Award, Dr. Carroll will investigate why these particular synapses are destroyed in lupus and how shutting off interferon could protect against damage to the central nervous system.

According to Dr. Carroll, "the study is transformative as it not only suggests a new approach to treatment, but also provides a mechanism for tracking the disease in people with lupus."

Excess Interferon-Beta May Trigger a Very Early Stage of Lupus Development

Dr. Mountz found that patients with high levels of the molecule interferon beta (IFN-β) within their early developing ("baby") B cells (the immune cells that grow to become autoantibody-producing cells) are more likely to have higher levels of autoantibodies and kidney disease. Among those individuals, African American patients, who are disproportionately affected by lupus, had higher levels IFN-β in these cells compared to Caucasian patients. Dr. Mountz will use his Distinguished Innovator Award to determine if the high level of IFN-β production within these baby B cells causes them to grow into adult autoantibody-producing B cells that trigger lupus.  

Dr. Mountz believes, "the results will form a solid foundation to develop treatments that block IFN-β for use in people with lupus and the identification of biological markers to identify lupus patients, especially among the African American population, at high risk of flares and kidney disease, who may respond to interferon therapies."

Dr. Mountz' groundbreaking work will provide further information for ongoing preclinical studies co-funded by the Lupus Research Alliance that are exploring IFN-β as a target for developing new therapies for lupus. 

Distinguished Innovator Award Honors Groundbreaking Research by Outstanding Scientists

The Distinguished Innovator Award was established in 2012 under the leadership of Dr. Bill Paul, the late Lupus Research Institute Scientific Advisory Board Chair. The Award encourages exceptional investigators worldwide to pursue innovative research projects that pair unconventional creativity with sound science to uncover the fundamental causes of lupus. Their research is expected to accelerate the development of novel treatments that prevent, arrest, or cure lupus and its complications.

Marilyn Paul, Dr. Paul's widow, presented the awards to Drs. Carroll and Mountz at the recent Lupus Research Alliance 2017 Forum for Discovery in New York City.

SOURCE Lupus Research Alliance

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