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Journal of Undergraduate Research

Keywords

Mutant Chemokine, inflammation, alzheimer's disease

College

Life Sciences

Department

Biology

Abstract

Alzheimer’s Disease (AD) is identified as a proteopathic disease that results from an extensive accumulation of amyloid plaques and neurofibrillary tangles in the brain. Several researchers have discovered that cerebrospinal fluid (CSF) contains biomarkers for AD such as Amyloid-beta and tau. Neuritic plaques in AD are surrounded by activated microglia and astrocytes which can initiate complement and inflammation in the presence of amyloid-beta. Macrophage inflammatory protein chemokine (C-C motif) ligand 4 (CCL4) is a biomarker found in CSF. A high level of expression is associated with risk of developing AD. CCL4 is expressed in a subpopulation of reactive astrocytes and microglia. Genome-wide Association study (GWAS) has identified a possible association between an atypical C-C motif chemokine receptor-like 2 (CCRL2) and CCL4. Mutation CCRL2-V180M shows to be statistically associated with decreased CSF CCL4 protein levels. However, due to the atypical nature of CCRL2, it has previously been suggested on a molecular level that CCRL2 and CCL4 do not interact. We hypothesized that the mutant CCRL2-V180M has altered binding affinity and functional response to CCL4.

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