Alzheimer's disease (AD) is the leading cause of dementia among elderly in the U.S. Over the past two decades, amyloid-beta, a small peptide found in the brains of Alzheimer's patients, is the indisputable culprit upstream of pathology and brain cell loss; hence, enormous effort has been made on developing amyloid-beta lowering strategies targeting its metabolism, aggregation or clearance. Despite the remarkable success of amyloid-beta-based therapies in preclinical animal studies, the overwhelming rate of these therapies has failed in human clinical trials. Thus, the complexity of this disease emphasizes the importance of investigating alternative targets to advance the AD field. Recent advances in the field strongly point out that inflammation in the brain plays a pivotal role in the pathogenesis of AD. Chronically activated inflammation and subsequent activation of brain cells called microglia may result in creating a harmful environment for neurons and potentially mediating the abnormal buildup of amyloid-beta and toxicity in the brain. Thus, successful cessation of overall brain inflammation is required to restore healthy inflammatory responses and mitigate inflammation-mediated toxicity. Our proposal takes an innovative and unique approach to investigate whether our novel pharmacological compound can activate factors to restore inflammatory responses to stead state levels, promote amyloid-beta clearance, and rescue mental function in a mouse model of AD. We propose to explore the therapeutic efficacy of the compound in a mouse model of AD and determine the proof-of-concept that modulating inflammation of the brain can play a pivotal role in rescuing the pathogenesis of AD.