Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer's disease
Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Soto, Ileana [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Umfang: |
11 |
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| Übergeordnetes Werk: |
Enthalten in: Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors - Zidane, Mustapha ELSEVIER, 2021, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:42 ; year:2016 ; pages:50-60 ; extent:11 |
| Links: |
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| DOI / URN: |
10.1016/j.neurobiolaging.2016.02.025 |
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| 520 | |a Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. | ||
| 520 | |a Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. | ||
| 650 | 7 | |a Neurodegeneration |2 Elsevier | |
| 650 | 7 | |a Neurovascular remodeling |2 Elsevier | |
| 650 | 7 | |a Aging |2 Elsevier | |
| 650 | 7 | |a Neurovascular deficits |2 Elsevier | |
| 700 | 1 | |a Grabowska, Weronika A. |4 oth | |
| 700 | 1 | |a Onos, Kristen D. |4 oth | |
| 700 | 1 | |a Graham, Leah C. |4 oth | |
| 700 | 1 | |a Jackson, Harriet M. |4 oth | |
| 700 | 1 | |a Simeone, Stephen N. |4 oth | |
| 700 | 1 | |a Howell, Gareth R. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Zidane, Mustapha ELSEVIER |t Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors |d 2021 |g Amsterdam [u.a.] |w (DE-627)ELV005660645 |
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10.1016/j.neurobiolaging.2016.02.025 doi GBVA2016008000028.pica (DE-627)ELV035232196 (ELSEVIER)S0197-4580(16)00184-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Soto, Ileana verfasserin aut Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer's disease 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Neurodegeneration Elsevier Neurovascular remodeling Elsevier Aging Elsevier Neurovascular deficits Elsevier Grabowska, Weronika A. oth Onos, Kristen D. oth Graham, Leah C. oth Jackson, Harriet M. oth Simeone, Stephen N. oth Howell, Gareth R. oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:42 year:2016 pages:50-60 extent:11 https://doi.org/10.1016/j.neurobiolaging.2016.02.025 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 42 2016 50-60 11 045F 610 |
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10.1016/j.neurobiolaging.2016.02.025 doi GBVA2016008000028.pica (DE-627)ELV035232196 (ELSEVIER)S0197-4580(16)00184-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Soto, Ileana verfasserin aut Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer's disease 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Neurodegeneration Elsevier Neurovascular remodeling Elsevier Aging Elsevier Neurovascular deficits Elsevier Grabowska, Weronika A. oth Onos, Kristen D. oth Graham, Leah C. oth Jackson, Harriet M. oth Simeone, Stephen N. oth Howell, Gareth R. oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:42 year:2016 pages:50-60 extent:11 https://doi.org/10.1016/j.neurobiolaging.2016.02.025 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 42 2016 50-60 11 045F 610 |
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10.1016/j.neurobiolaging.2016.02.025 doi GBVA2016008000028.pica (DE-627)ELV035232196 (ELSEVIER)S0197-4580(16)00184-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Soto, Ileana verfasserin aut Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer's disease 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Neurodegeneration Elsevier Neurovascular remodeling Elsevier Aging Elsevier Neurovascular deficits Elsevier Grabowska, Weronika A. oth Onos, Kristen D. oth Graham, Leah C. oth Jackson, Harriet M. oth Simeone, Stephen N. oth Howell, Gareth R. oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:42 year:2016 pages:50-60 extent:11 https://doi.org/10.1016/j.neurobiolaging.2016.02.025 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 42 2016 50-60 11 045F 610 |
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10.1016/j.neurobiolaging.2016.02.025 doi GBVA2016008000028.pica (DE-627)ELV035232196 (ELSEVIER)S0197-4580(16)00184-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Soto, Ileana verfasserin aut Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer's disease 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Neurodegeneration Elsevier Neurovascular remodeling Elsevier Aging Elsevier Neurovascular deficits Elsevier Grabowska, Weronika A. oth Onos, Kristen D. oth Graham, Leah C. oth Jackson, Harriet M. oth Simeone, Stephen N. oth Howell, Gareth R. oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:42 year:2016 pages:50-60 extent:11 https://doi.org/10.1016/j.neurobiolaging.2016.02.025 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 42 2016 50-60 11 045F 610 |
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10.1016/j.neurobiolaging.2016.02.025 doi GBVA2016008000028.pica (DE-627)ELV035232196 (ELSEVIER)S0197-4580(16)00184-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Soto, Ileana verfasserin aut Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer's disease 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. Neurodegeneration Elsevier Neurovascular remodeling Elsevier Aging Elsevier Neurovascular deficits Elsevier Grabowska, Weronika A. oth Onos, Kristen D. oth Graham, Leah C. oth Jackson, Harriet M. oth Simeone, Stephen N. oth Howell, Gareth R. oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:42 year:2016 pages:50-60 extent:11 https://doi.org/10.1016/j.neurobiolaging.2016.02.025 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 42 2016 50-60 11 045F 610 |
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Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer's disease |
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Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. |
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Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. |
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Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD. |
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Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer's disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APB Tg ) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APB Tg mice that carry only one copy of Meox2 (B6.APB Tg .Mx −/+ ) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APB Tg mice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Neurodegeneration</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Neurovascular remodeling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Aging</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Neurovascular deficits</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Grabowska, Weronika A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Onos, Kristen D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Graham, Leah C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jackson, Harriet M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Simeone, Stephen N.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Howell, Gareth R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Zidane, Mustapha ELSEVIER</subfield><subfield code="t">Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors</subfield><subfield code="d">2021</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV005660645</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:42</subfield><subfield code="g">year:2016</subfield><subfield code="g">pages:50-60</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.neurobiolaging.2016.02.025</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GEO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-AST</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">38.70</subfield><subfield code="j">Geophysik: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">39.53</subfield><subfield code="j">Planeten</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">42</subfield><subfield code="j">2016</subfield><subfield code="h">50-60</subfield><subfield code="g">11</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
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