Alzheimer disease is the most common cause of dementia, afflicting 24 million people worldwide. Over time, Alzheimer’s disease gradually destroys a person’s memory and ability to learn and carry out daily activities. In addition; individuals may also experience changes in personality and behavior. Alzheimer disease is accompanied by the presence of amyloid plaques and neurofibrillary tangles in the brain of Alzheimer’s patients with increases in pro-inflammatory cytokines. Beta-amyloid is a key protein shown to play a central role in Alzheimer’s disease etiology. Unfortunately, there is currently no known cure, finding a way to stop Beta-amyloid production and/or increase it degradation will lead to a potentially drug target that can be used to stop the disease. Researchers at the Roskamp Institute showed that inhibition of a Pro-inflammatory cytokine; the granulocyte macrophage colony stimulating factor (GM-CSF) a category of signaling proteins used extensively in cellular communication. GM-CSF has been suggested to induce programmed cell death in the brain tissue of patients with dementia once secreted. Scientist at the Roskamp institute showed that blocking this protein reduce the production of the main pathological protein that causes Alzheimer’s disease (beta-Amyloid) below basal level. In addition the Roskamp Institute scientists examined the mechanism underlying Beta-amyloid reduction after silencing of the receptor protein of G-CSF. Their result show that these effect is due to the fact that blocking the GM-CSF receptor reduce APP (Beta-amyloid protein precursor) trafficking from the cell membrane to the inside of the cell were the preotein in cleaved to generate the beta-Amyloid fragment. The discovery is detailed in an article appears in the journal Cytokine.