Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease

Alzheimer's 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 incl...
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Autor*in:	Liza Bergkvist [verfasserIn] Zhen Du [verfasserIn] Greta Elovsson [verfasserIn] Hanna Appelqvist [verfasserIn] Laura S. Itzhaki [verfasserIn] Janet R. Kumita [verfasserIn] Katarina Kågedal [verfasserIn] Ann‐Christin Brorsson [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration

Übergeordnetes Werk:	In: FEBS Open Bio - Wiley, 2013, 10(2020), 3, Seite 338-350
Übergeordnetes Werk:	volume:10 ; year:2020 ; number:3 ; pages:338-350

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1002/2211-5463.12773

Katalog-ID:	DOAJ002230194

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520			\|a Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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.
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allfields	10.1002/2211-5463.12773 doi (DE-627)DOAJ002230194 (DE-599)DOAJd3371f795ac8455391516ee6c99ced82 DE-627 ger DE-627 rakwb eng QH301-705.5 Liza Bergkvist verfasserin aut Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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. Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration Biology (General) Zhen Du verfasserin aut Greta Elovsson verfasserin aut Hanna Appelqvist verfasserin aut Laura S. Itzhaki verfasserin aut Janet R. Kumita verfasserin aut Katarina Kågedal verfasserin aut Ann‐Christin Brorsson verfasserin aut In FEBS Open Bio Wiley, 2013 10(2020), 3, Seite 338-350 (DE-627)686948351 (DE-600)2651702-4 22115463 nnns volume:10 year:2020 number:3 pages:338-350 https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/article/d3371f795ac8455391516ee6c99ced82 kostenfrei https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/toc/2211-5463 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2020 3 338-350
spelling	10.1002/2211-5463.12773 doi (DE-627)DOAJ002230194 (DE-599)DOAJd3371f795ac8455391516ee6c99ced82 DE-627 ger DE-627 rakwb eng QH301-705.5 Liza Bergkvist verfasserin aut Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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. Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration Biology (General) Zhen Du verfasserin aut Greta Elovsson verfasserin aut Hanna Appelqvist verfasserin aut Laura S. Itzhaki verfasserin aut Janet R. Kumita verfasserin aut Katarina Kågedal verfasserin aut Ann‐Christin Brorsson verfasserin aut In FEBS Open Bio Wiley, 2013 10(2020), 3, Seite 338-350 (DE-627)686948351 (DE-600)2651702-4 22115463 nnns volume:10 year:2020 number:3 pages:338-350 https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/article/d3371f795ac8455391516ee6c99ced82 kostenfrei https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/toc/2211-5463 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2020 3 338-350
allfields_unstemmed	10.1002/2211-5463.12773 doi (DE-627)DOAJ002230194 (DE-599)DOAJd3371f795ac8455391516ee6c99ced82 DE-627 ger DE-627 rakwb eng QH301-705.5 Liza Bergkvist verfasserin aut Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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. Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration Biology (General) Zhen Du verfasserin aut Greta Elovsson verfasserin aut Hanna Appelqvist verfasserin aut Laura S. Itzhaki verfasserin aut Janet R. Kumita verfasserin aut Katarina Kågedal verfasserin aut Ann‐Christin Brorsson verfasserin aut In FEBS Open Bio Wiley, 2013 10(2020), 3, Seite 338-350 (DE-627)686948351 (DE-600)2651702-4 22115463 nnns volume:10 year:2020 number:3 pages:338-350 https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/article/d3371f795ac8455391516ee6c99ced82 kostenfrei https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/toc/2211-5463 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2020 3 338-350
allfieldsGer	10.1002/2211-5463.12773 doi (DE-627)DOAJ002230194 (DE-599)DOAJd3371f795ac8455391516ee6c99ced82 DE-627 ger DE-627 rakwb eng QH301-705.5 Liza Bergkvist verfasserin aut Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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. Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration Biology (General) Zhen Du verfasserin aut Greta Elovsson verfasserin aut Hanna Appelqvist verfasserin aut Laura S. Itzhaki verfasserin aut Janet R. Kumita verfasserin aut Katarina Kågedal verfasserin aut Ann‐Christin Brorsson verfasserin aut In FEBS Open Bio Wiley, 2013 10(2020), 3, Seite 338-350 (DE-627)686948351 (DE-600)2651702-4 22115463 nnns volume:10 year:2020 number:3 pages:338-350 https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/article/d3371f795ac8455391516ee6c99ced82 kostenfrei https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/toc/2211-5463 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2020 3 338-350
allfieldsSound	10.1002/2211-5463.12773 doi (DE-627)DOAJ002230194 (DE-599)DOAJd3371f795ac8455391516ee6c99ced82 DE-627 ger DE-627 rakwb eng QH301-705.5 Liza Bergkvist verfasserin aut Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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. Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration Biology (General) Zhen Du verfasserin aut Greta Elovsson verfasserin aut Hanna Appelqvist verfasserin aut Laura S. Itzhaki verfasserin aut Janet R. Kumita verfasserin aut Katarina Kågedal verfasserin aut Ann‐Christin Brorsson verfasserin aut In FEBS Open Bio Wiley, 2013 10(2020), 3, Seite 338-350 (DE-627)686948351 (DE-600)2651702-4 22115463 nnns volume:10 year:2020 number:3 pages:338-350 https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/article/d3371f795ac8455391516ee6c99ced82 kostenfrei https://doi.org/10.1002/2211-5463.12773 kostenfrei https://doaj.org/toc/2211-5463 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2020 3 338-350
language	English
source	In FEBS Open Bio 10(2020), 3, Seite 338-350 volume:10 year:2020 number:3 pages:338-350
sourceStr	In FEBS Open Bio 10(2020), 3, Seite 338-350 volume:10 year:2020 number:3 pages:338-350
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration Biology (General)
isfreeaccess_bool	true
container_title	FEBS Open Bio
authorswithroles_txt_mv	Liza Bergkvist @@aut@@ Zhen Du @@aut@@ Greta Elovsson @@aut@@ Hanna Appelqvist @@aut@@ Laura S. Itzhaki @@aut@@ Janet R. Kumita @@aut@@ Katarina Kågedal @@aut@@ Ann‐Christin Brorsson @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	686948351
id	DOAJ002230194
language_de	englisch
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In the Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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. 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callnumber-first	Q - Science
author	Liza Bergkvist
spellingShingle	Liza Bergkvist misc QH301-705.5 misc Alzheimer's disease misc amyloid‐β misc Drosophila melanogaster misc endo‐lysosomal system misc neurodegeneration misc Biology (General) Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease
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topic_title	QH301-705.5 Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease Alzheimer's disease amyloid‐β Drosophila melanogaster endo‐lysosomal system neurodegeneration
topic	misc QH301-705.5 misc Alzheimer's disease misc amyloid‐β misc Drosophila melanogaster misc endo‐lysosomal system misc neurodegeneration misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc Alzheimer's disease misc amyloid‐β misc Drosophila melanogaster misc endo‐lysosomal system misc neurodegeneration misc Biology (General)
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title	Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease
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title_full	Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease
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author_browse	Liza Bergkvist Zhen Du Greta Elovsson Hanna Appelqvist Laura S. Itzhaki Janet R. Kumita Katarina Kågedal Ann‐Christin Brorsson
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title_sort	mapping pathogenic processes contributing to neurodegeneration in drosophila models of alzheimer's disease
callnumber	QH301-705.5
title_auth	Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease
abstract	Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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.
abstractGer	Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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.
abstract_unstemmed	Alzheimer's 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 Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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.
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title_short	Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease
url	https://doi.org/10.1002/2211-5463.12773 https://doaj.org/article/d3371f795ac8455391516ee6c99ced82 https://doaj.org/toc/2211-5463
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author2	Zhen Du Greta Elovsson Hanna Appelqvist Laura S. Itzhaki Janet R. Kumita Katarina Kågedal Ann‐Christin Brorsson
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up_date	2024-07-04T00:24:18.059Z
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Appropriate disease models are necessary to investigate disease mechanisms and potential treatments. Drosophila melanogaster models of AD include the Aβ fly model and the AβPP‐BACE1 fly model. In the Aβ fly model, the Aβ peptide is fused to a secretion sequence and directly overexpressed. In the AβPP‐BACE1 model, human AβPP and human BACE1 are expressed in the fly, resulting in in vivo production of Aβ peptides and other AβPP 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 Aβ fly model, this correlates with high Aβ1–42 levels and down‐regulation of the levels of mRNA encoding lysosomal‐associated membrane protein 1, lamp1 (a lysosomal marker), while in the AβPP‐BACE1 fly model, neuronal cell death correlates with low Aβ1–42 levels, up‐regulation of lamp1 mRNA levels and increased levels of C‐terminal fragments. In addition, a significant amount of AβPP/Aβ antibody (4G8)‐positive species, located close to the endosomal marker rab5, was detected in the AβPP‐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. 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Mapping pathogenic processes contributing to neurodegeneration in Drosophila models of Alzheimer's disease

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