ArticleScientific reports2015
Loss of Polo ameliorates APP-induced Alzheimer's disease-like symptoms in Drosophila.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Histone deacetylase SIRT6 regulates tryptophan catabolism and prevents metabolite imbalance associated with neurodegeneration.Nature communications · 2025Article
- The inter-organelle cross-talk finely orchestrated in the amyloidogenic processing of amyloid precursor protein in dendritic arborization neurons ofTheranostics · 2025Article
- Alzheimer's disease pathophysiology in the Retina.Progress in retinal and eye research · 2024Review
- Miro, a Rho GTPase genetically interacts with Alzheimer's disease-associated genes (Biology open · 2020Article
- CHIP modulates APP-induced autophagy-dependent pathological symptoms in Drosophila.Aging cell · 2020Article
- Genetic Dissection of Alzheimer's Disease UsingInternational journal of molecular sciences · 2020Review
- Glioblastoma cells vampirize WNT from neurons and trigger a JNK/MMP signaling loop that enhances glioblastoma progression and neurodegeneration.PLoS biology · 2019Article
- UsingBioMed research international · 2018Review
- Insulin Signaling in the Peripheral and Central Nervous System Regulates Female Sexual Receptivity during Starvation inFrontiers in physiology · 2017Article
- dFoxO promotes Wingless signaling in Drosophila.Scientific reports · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The amyloid precursor protein (APP) has been implicated in the pathogenesis of Alzheimer's disease (AD). Despite extensive studies, little is known about the regulation of APP's functions in vivo. Here we report that expression of human APP in Drosophila, in the same temporal-spatial pattern as its homolog APPL, induced morphological defects in wings and larval NMJ, larva and adult locomotion dysfunctions, male choice disorder and lifespan shortening. To identify additional genes that modulate APP functions, we performed a genetic screen and found that loss of Polo, a key regulator of cell cycle, partially suppressed APP-induced morphological and behavioral defects in larval and adult stages. Finally, we showed that eye-specific expression of APP induced retina degeneration and cell cycle re-entry, both phenotypes were mildly ameliorated by loss of Polo. These results suggest Polo is an important in vivo regulator of the pathological functions of APP, and provide insight into the role of cell cycle re-entry in AD pathogenesis.
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