In the quest for understanding human neurodegenerative disorders, a variety of organisms have been used to create disease models. Because of its many advantages, Drosophila melanogaster is currently being used to model many human conditions including poly Q expansion disorders such as Huntington’s disease, Parkinson’s disease, Alzheimer’s disease (AD), and other dementias. AD is characterized by two pathologies; the first, extracellular amyloid β (Aβ) plaques, consist mainly of toxic Aβ42 peptide, and the second, intracellular neurofibrillary tangles, consists mainly of hyperphosphorylated tau protein. Drosophila AD models have focused either on replicating the amyloid precursor protein (APP) processing model (Aβ is a proteolytic product of APP) or on expression of simpler secreted Aβ peptides in the fly nervous system. These models replicate many of the features of human AD, including Aβ deposition, neuronal loss and neurodegeneration, and behavioral phenotypes such as impaired learning and memory. In recent years, following the characterization of these models, focus has shifted to utilizing the genetic power of Drosophila and screens are being conducted for identifying modifiers of AD pathology.