Moreover, APPPS1 mice lacking C3 had fewer plaque-associated astrocytes and microglia, improved cognitive function, and were protected from an age-dependent loss of synapses and neurons, despite an increase in Aβ plaques compared to APP/PS1 mice expressing C3 [89], suggesting the aberrant upregulation of the complement system can contribute to AD disease progression. The gene discussed is APP; the disease is Alzheimer disease.