Alzheimer’s disease is a chronic neurodegenerative disease and a major cause of dementia. Early symptoms include short-term memory loss; as the disease advances, symptoms progressively worsen and include cognitive decline, disorientation, and ultimately loss of body function and death. The disease involves accumulation of plaques in the brain, which are characterized by the deposition of a protein called amyloid beta.
Relatively recent research has shown the immune system—specifically microglia—is an important component of AD. These are immune cells interspersed throughout the brain throughout the lifetime among and between the neurons. Microglia participate in many normal functions, but also can be critical in AD. Understanding microglia in AD is necessary and may uncover previously unknown pathways by which the immune system promotes or protects against AD.
A powerful strategy to delve into microglial function involves identifying the key molecules that control microglial development, survival and behavior. Preliminary data suggest a specific molecule, a growth factor and cytokine called IL-3, activates microglial cells, instructing them to remove harmful amyloid beta plaques. In the absence of IL-3, however, microglia are unable to find such plaques, which worsens disease. IL-3, therefore, might be an important therapeutic target in AD, and this research seeks to elucidate IL-3’s role in animal models of AD.