Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimers disease

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Bergkvist, LizaLinköpings universitet,Kemi,Tekniska fakulteten,Van Andel Res Inst, MI USA (author)

Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimers disease

Article/chapterEnglish2020

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2020-01-22
WILEY,2020
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LIBRIS-ID:oai:DiVA.org:liu-163625
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-163625URI
https://doi.org/10.1002/2211-5463.12773DOI

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Language:English
Summary in:English

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Subject category:art swepub-publicationtype

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Funding Agencies|Torsten Soderberg Foundation; Apotekare Hedbergs Foundation; Ahlens Foundation; Swedish Alzheimer Foundation; Swedish Dementia Foundation; Frimurarestiftelsen; Centre for Misfolding Diseases; Herchel Smith PhD Research Scholarship; Rosetrees TrustRosetrees Trust
Alzheimers disease (AD) is the most common form of dementia, affecting millions of people and currently lacking available disease-modifying treatments. Appropriate disease models are necessary to investigate disease mechanisms and potential treatments. Drosophila melanogaster models of AD include the A beta fly model and the A beta PP-BACE1 fly model. In the A beta fly model, the A beta peptide is fused to a secretion sequence and directly overexpressed. In the A beta PP-BACE1 model, human A beta PP and human BACE1 are expressed in the fly, resulting in in vivo production of A beta peptides and other A beta PP cleavage products. Although these two models have been used for almost two decades, the underlying mechanisms resulting in neurodegeneration are not yet clearly understood. In this study, we have characterized toxic mechanisms in these two AD fly models. We detected neuronal cell death and increased protein carbonylation (indicative of oxidative stress) in both AD fly models. In the A beta fly model, this correlates with high A beta(1-42) levels and down-regulation of the levels of mRNA encoding lysosomal-associated membrane protein 1, lamp1 (a lysosomal marker), while in the A beta PP-BACE1 fly model, neuronal cell death correlates with low A beta(1-42) levels, up-regulation of lamp1 mRNA levels and increased levels of C-terminal fragments. In addition, a significant amount of A beta PP/A beta antibody (4G8)-positive species, located close to the endosomal marker rab5, was detected in the A beta PP-BACE1 model. Taken together, this study highlights the similarities and differences in the toxic mechanisms which result in neuronal death in two different AD fly models. Such information is important to consider when utilizing these models to study AD pathogenesis or screening for potential treatments.

Subject headings and genre

NATURVETENSKAP Biologi Strukturbiologi hsv//swe
NATURAL SCIENCES Biological Sciences Structural Biology hsv//eng
Alzheimers disease; amyloid-beta; Drosophila melanogaster; endo-lysosomal system; neurodegeneration

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Du, ZhenUniv Cambridge, England; Univ Cambridge, England (author)
Elovsson, GretaLinköpings universitet,Kemi,Tekniska fakulteten(Swepub:liu)greel03 (author)
Appelqvist, HannaLinköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten(Swepub:liu)hanmi48 (author)
Itzhaki, Laura S.Univ Cambridge, England (author)
Kumita, Janet R.Univ Cambridge, England (author)
Kågedal, KatarinaLinköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten(Swepub:liu)katka10 (author)
Brorsson, Ann-ChristinLinköpings universitet,Kemi,Tekniska fakulteten(Swepub:liu)annbr05 (author)
Linköpings universitetKemi (creator_code:org_t)

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In:FEBS Open Bio: WILEY10:3, s. 338-3502211-5463

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By the author/editor: Bergkvist, Liza; Du, Zhen; Elovsson, Greta; Appelqvist, Hann ...; Itzhaki, Laura S ...; Kumita, Janet R.; show more...; Kågedal, Katarin ...; Brorsson, Ann-Ch ...; show less...

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