Alzheimer's disease (AD) is the leading cause of dementia and a top 10 cause of death in the United States. More than 6 million Americans currently suffer from AD. This complex degenerative condition is caused by both genetic and environmental risk factors. Neuroinflammation plays a critical role in the progression of AD and excessive neuroinflammation can be initiated by chemokine signaling within the brain. A genome-wide association study surveyed 59 AD-related proteins and their correlation with chemokines. One chemokine, chemokine ligand 4 (CCL4), was found at lower concentrations to correlation with the C-C chemokine receptor-like 2 variant V140M (CCRL2-V140M). Increased CCL4 levels are a risk factor for AD and CCRL2-V140M could provide insights into AD development protection. CCRL2 is a seven-transmembrane domain receptor from the atypical chemokine receptor family, receptors that modulate the inflammatory response by modifying chemokine availability. CCRL2's only known binding partner is chemerin. We performed in-silico and in-vitro binding analyses of CCL4 and chemerin to CCRL2-WT and CCRL23-V140M and found no differences in binding affinity, suggesting a non-direct mode of action may distinguish the CCRL2 variant and WT. Further work is needed to explain the inverse association between CCRL2-V140M and CCL4.
University / Institution: Brigham Young University
Format: In Person
SESSION C (1:45-3:15PM)
Area of Research: Science & Technology
Faculty Mentor: Scott Weber
Location: Alumni House, DUMKE ROOM (2:25pm)