In our recent paper we show that neuronal loss in Alzheimer’s disease is the result of a cell quality control mechanism trying to protect the brain from the accumulation of malfunctioning neurons. We have generated fruit flies that express in their brain the human amyloid-beta protein, that forms aggregates in the brains of AD patients. The formation of amyloid-β aggregates in the brain is a crucial step in the development of AD.
These Alzheimer flies display symptoms and pathologies similar to those of AD patients: they show loss of long-term memory, accelerated aging of the brain and motor coordination problems (Movie 1 below). If the culling of malfunctioning neurons is enhanced in this fly model of Alzheimer’s disease, the development of motor and cognitive defects is strongly delayed (see Movie 2).
Movie 1: Walking and orientation of Alzheimer flies
Movie 2: Walking of Alzheimer flies where removal of unfit neurons has been enhanced