Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease
Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression pro...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Janssen, Leen [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
11 |
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| Übergeordnetes Werk: |
Enthalten in: Mixed polymer brushes with integrated antibacterial and antifouling properties - Fu, Yanhong ELSEVIER, 2019, BBA, Amsterdam |
|---|---|
| Übergeordnetes Werk: |
volume:1863 ; year:2017 ; number:2 ; pages:395-405 ; extent:11 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.bbadis.2016.11.014 |
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| 520 | |a Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. | ||
| 520 | |a Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. | ||
| 700 | 1 | |a Dubbelaar, Marissa L. |4 oth | |
| 700 | 1 | |a Holtman, Inge R. |4 oth | |
| 700 | 1 | |a de Boer-Bergsma, Jelkje |4 oth | |
| 700 | 1 | |a Eggen, Bart J.L. |4 oth | |
| 700 | 1 | |a Boddeke, Hendrikus W.G.M. |4 oth | |
| 700 | 1 | |a De Deyn, Peter P. |4 oth | |
| 700 | 1 | |a Van Dam, Debby |4 oth | |
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10.1016/j.bbadis.2016.11.014 doi GBVA2017014000010.pica (DE-627)ELV015223523 (ELSEVIER)S0925-4439(16)30296-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Janssen, Leen verfasserin aut Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Dubbelaar, Marissa L. oth Holtman, Inge R. oth de Boer-Bergsma, Jelkje oth Eggen, Bart J.L. oth Boddeke, Hendrikus W.G.M. oth De Deyn, Peter P. oth Van Dam, Debby oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1863 year:2017 number:2 pages:395-405 extent:11 https://doi.org/10.1016/j.bbadis.2016.11.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1863 2017 2 395-405 11 045F 570 |
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10.1016/j.bbadis.2016.11.014 doi GBVA2017014000010.pica (DE-627)ELV015223523 (ELSEVIER)S0925-4439(16)30296-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Janssen, Leen verfasserin aut Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Dubbelaar, Marissa L. oth Holtman, Inge R. oth de Boer-Bergsma, Jelkje oth Eggen, Bart J.L. oth Boddeke, Hendrikus W.G.M. oth De Deyn, Peter P. oth Van Dam, Debby oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1863 year:2017 number:2 pages:395-405 extent:11 https://doi.org/10.1016/j.bbadis.2016.11.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1863 2017 2 395-405 11 045F 570 |
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10.1016/j.bbadis.2016.11.014 doi GBVA2017014000010.pica (DE-627)ELV015223523 (ELSEVIER)S0925-4439(16)30296-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Janssen, Leen verfasserin aut Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Dubbelaar, Marissa L. oth Holtman, Inge R. oth de Boer-Bergsma, Jelkje oth Eggen, Bart J.L. oth Boddeke, Hendrikus W.G.M. oth De Deyn, Peter P. oth Van Dam, Debby oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1863 year:2017 number:2 pages:395-405 extent:11 https://doi.org/10.1016/j.bbadis.2016.11.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1863 2017 2 395-405 11 045F 570 |
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10.1016/j.bbadis.2016.11.014 doi GBVA2017014000010.pica (DE-627)ELV015223523 (ELSEVIER)S0925-4439(16)30296-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Janssen, Leen verfasserin aut Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Dubbelaar, Marissa L. oth Holtman, Inge R. oth de Boer-Bergsma, Jelkje oth Eggen, Bart J.L. oth Boddeke, Hendrikus W.G.M. oth De Deyn, Peter P. oth Van Dam, Debby oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1863 year:2017 number:2 pages:395-405 extent:11 https://doi.org/10.1016/j.bbadis.2016.11.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1863 2017 2 395-405 11 045F 570 |
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10.1016/j.bbadis.2016.11.014 doi GBVA2017014000010.pica (DE-627)ELV015223523 (ELSEVIER)S0925-4439(16)30296-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 540 VZ 52.78 bkl Janssen, Leen verfasserin aut Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. Dubbelaar, Marissa L. oth Holtman, Inge R. oth de Boer-Bergsma, Jelkje oth Eggen, Bart J.L. oth Boddeke, Hendrikus W.G.M. oth De Deyn, Peter P. oth Van Dam, Debby oth Enthalten in Elsevier Fu, Yanhong ELSEVIER Mixed polymer brushes with integrated antibacterial and antifouling properties 2019 BBA Amsterdam (DE-627)ELV001872222 volume:1863 year:2017 number:2 pages:395-405 extent:11 https://doi.org/10.1016/j.bbadis.2016.11.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 52.78 Oberflächentechnik Wärmebehandlung VZ AR 1863 2017 2 395-405 11 045F 570 |
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Janssen, Leen @@aut@@ Dubbelaar, Marissa L. @@oth@@ Holtman, Inge R. @@oth@@ de Boer-Bergsma, Jelkje @@oth@@ Eggen, Bart J.L. @@oth@@ Boddeke, Hendrikus W.G.M. @@oth@@ De Deyn, Peter P. @@oth@@ Van Dam, Debby @@oth@@ |
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Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease |
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Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. |
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Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. |
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Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice. |
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