RRC ID 53923
著者 Furotani K, Kamimura K, Yajima T, Nakayama M, Enomoto R, Tamura T, Okazawa H, Sone M.
タイトル Suppression of the synaptic localization of a subset of proteins including APP partially ameliorates phenotypes of the Drosophila Alzheimer's disease model.
ジャーナル PLoS One
Abstract APP (amyloid precursor protein), the causative molecule of Alzheimer's disease, is synthesized in neuronal cell bodies and subsequently transported to synapses. We previously showed that the yata gene is required for the synaptic transport of the APP orthologue in Drosophila melanogaster. In this study, we examined the effect of a reduction in yata expression in the Drosophila Alzheimer's disease model, in which expression of human mutant APP was induced. The synaptic localization of APP and other synaptic proteins was differentially inhibited by yata knockdown and null mutation. Expression of APP resulted in abnormal synaptic morphology and the premature death of animals. These phenotypes were partially but significantly rescued by yata knockdown, whereas yata knockdown itself caused no abnormality. Moreover, we observed that synaptic transmission accuracy was impaired in our model, and this phenotype was improved by yata knockdown. Thus, our data suggested that the phenotypes caused by APP can be partially prevented by inhibition of the synaptic localization of a subset of synaptic proteins including APP.
巻・号 13(9)
ページ e0204048
公開日 2018-9-18
DOI 10.1371/journal.pone.0204048
PII PONE-D-18-13146
PMID 30226901
PMC PMC6143267
MeSH Alzheimer Disease / metabolism* Alzheimer Disease / prevention & control Amyloid beta-Protein Precursor / metabolism* Animals Disease Models, Animal Drosophila Proteins / genetics Drosophila melanogaster / genetics Drosophila melanogaster / metabolism* Female Gene Knockdown Techniques Male Nerve Tissue Proteins / metabolism Protein Kinases / genetics Synapses / metabolism*
IF 2.74
引用数 2
リソース情報
ショウジョウバエ 1973R-3