In order to further determine whether the gain of LC3B function in astrocytes can ameliorate the Aβ-associated pathology in an animal model of AD, we transduced AAV with GFAP promoter-driven LC3B overexpression vector (AAV-pGFAP-LC3B) to the hippocampus of WT and APP/PS1 mice. This evidence concerns the gene APP and Alzheimer disease.