Amyloid-β peptides slightly affect lifespan or antimicrobial peptide gene expression in Drosophila melanogaster

BMC Genetics

Mikhail V. Shaposhnikov¹  Vladimir A. Mitkevich¹  Olga I. Kechko¹  Alexey А. Moskalev¹  Alexander A. Makarov¹  Nadezhda V. Zemskaya²  Lyubov А. Koval²  Natalya R. Minnikhanova² 

[1]Engelhardt Institute of Molecular Biology, Russian Academy of Sciences

[2]Institute of Biology of Komi Science Center of Ural Branch of RAS

关键词: Lifespan;    Aging;    Drosophila melanogaster;    Amyloid-β peptides;    Antimicrobial peptides;    Transcription factor FOXO;   

DOI  :  10.1186/s12863-020-00866-y

来源: DOAJ

【 摘 要 】

Abstract Background Beta-amyloid peptide (Aβ) is the key protein in the pathogenesis of Alzheimer’s disease, the most common age-related neurodegenerative disorder in humans. Aβ peptide induced pathological phenotypes in different model organisms include neurodegeneration and lifespan decrease. However, recent experimental evidence suggests that Aβ may utilize oligomerization and fibrillization to function as an antimicrobial peptide (AMP), and protect the host from infections. We used the power of Drosophila model to study mechanisms underlying a dual role for Aβ peptides. Results We investigated the effects of Drosophila treatment with three Aβ42 peptide isoforms, which differ in their ability to form oligomers and aggregates on the lifespan, locomotor activity and AMP genes expression. Aβ42 slightly decreased female’s median lifespan (by 4.5%), but the effect was not related to the toxicity of peptide isoform. The lifespan and relative levels of AMP gene expression in male flies as well as locomotor activity in both sexes were largely unaffected by Aβ42 peptide treatment. Regardless of the effects on lifespan, Aβ42 peptide treatment induced decrease in AMP genes expression in females, but the effects were not robust. Conclusions The results demonstrate that chronic treatment with Aβ42 peptides does not drastically affect fly aging or immunity.

【 授权许可】

Unknown