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). 

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Movie 1: Walking and orientation of Alzheimer flies

Movie 2: Walking of Alzheimer flies where removal of unfit neurons has been enhanced