High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology
Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, t...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Gratuze, Maud [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Schlagwörter: |
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| Umfang: |
3 |
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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.] |
|---|---|
| Übergeordnetes Werk: |
volume:47 ; year:2016 ; pages:71-73 ; extent:3 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.neurobiolaging.2016.07.016 |
|---|
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| 520 | |a Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. | ||
| 520 | |a Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. | ||
| 650 | 7 | |a High-cholesterol diet |2 Elsevier | |
| 650 | 7 | |a High-sugar diet |2 Elsevier | |
| 650 | 7 | |a Obesity |2 Elsevier | |
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| 700 | 1 | |a Marette, André |4 oth | |
| 700 | 1 | |a Planel, Emmanuel |4 oth | |
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10.1016/j.neurobiolaging.2016.07.016 doi GBVA2016008000029.pica (DE-627)ELV024371181 (ELSEVIER)S0197-4580(16)30153-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Gratuze, Maud verfasserin aut High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology 2016transfer abstract 3 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. High-cholesterol diet Elsevier High-sugar diet Elsevier Obesity Elsevier Tau protein Elsevier High-fat diet Elsevier Diabetes Elsevier Tauopathy Elsevier Alzheimer's disease Elsevier Western diet Elsevier Julien, Jacinthe oth Morin, Françoise oth Calon, Frédéric oth Hébert, Sébastien S. oth Marette, André oth Planel, Emmanuel 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:47 year:2016 pages:71-73 extent:3 https://doi.org/10.1016/j.neurobiolaging.2016.07.016 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 47 2016 71-73 3 045F 610 |
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10.1016/j.neurobiolaging.2016.07.016 doi GBVA2016008000029.pica (DE-627)ELV024371181 (ELSEVIER)S0197-4580(16)30153-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Gratuze, Maud verfasserin aut High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology 2016transfer abstract 3 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. High-cholesterol diet Elsevier High-sugar diet Elsevier Obesity Elsevier Tau protein Elsevier High-fat diet Elsevier Diabetes Elsevier Tauopathy Elsevier Alzheimer's disease Elsevier Western diet Elsevier Julien, Jacinthe oth Morin, Françoise oth Calon, Frédéric oth Hébert, Sébastien S. oth Marette, André oth Planel, Emmanuel 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:47 year:2016 pages:71-73 extent:3 https://doi.org/10.1016/j.neurobiolaging.2016.07.016 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 47 2016 71-73 3 045F 610 |
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10.1016/j.neurobiolaging.2016.07.016 doi GBVA2016008000029.pica (DE-627)ELV024371181 (ELSEVIER)S0197-4580(16)30153-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Gratuze, Maud verfasserin aut High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology 2016transfer abstract 3 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. High-cholesterol diet Elsevier High-sugar diet Elsevier Obesity Elsevier Tau protein Elsevier High-fat diet Elsevier Diabetes Elsevier Tauopathy Elsevier Alzheimer's disease Elsevier Western diet Elsevier Julien, Jacinthe oth Morin, Françoise oth Calon, Frédéric oth Hébert, Sébastien S. oth Marette, André oth Planel, Emmanuel 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:47 year:2016 pages:71-73 extent:3 https://doi.org/10.1016/j.neurobiolaging.2016.07.016 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 47 2016 71-73 3 045F 610 |
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10.1016/j.neurobiolaging.2016.07.016 doi GBVA2016008000029.pica (DE-627)ELV024371181 (ELSEVIER)S0197-4580(16)30153-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Gratuze, Maud verfasserin aut High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology 2016transfer abstract 3 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. High-cholesterol diet Elsevier High-sugar diet Elsevier Obesity Elsevier Tau protein Elsevier High-fat diet Elsevier Diabetes Elsevier Tauopathy Elsevier Alzheimer's disease Elsevier Western diet Elsevier Julien, Jacinthe oth Morin, Françoise oth Calon, Frédéric oth Hébert, Sébastien S. oth Marette, André oth Planel, Emmanuel 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:47 year:2016 pages:71-73 extent:3 https://doi.org/10.1016/j.neurobiolaging.2016.07.016 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 47 2016 71-73 3 045F 610 |
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10.1016/j.neurobiolaging.2016.07.016 doi GBVA2016008000029.pica (DE-627)ELV024371181 (ELSEVIER)S0197-4580(16)30153-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Gratuze, Maud verfasserin aut High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology 2016transfer abstract 3 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. High-cholesterol diet Elsevier High-sugar diet Elsevier Obesity Elsevier Tau protein Elsevier High-fat diet Elsevier Diabetes Elsevier Tauopathy Elsevier Alzheimer's disease Elsevier Western diet Elsevier Julien, Jacinthe oth Morin, Françoise oth Calon, Frédéric oth Hébert, Sébastien S. oth Marette, André oth Planel, Emmanuel 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:47 year:2016 pages:71-73 extent:3 https://doi.org/10.1016/j.neurobiolaging.2016.07.016 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 47 2016 71-73 3 045F 610 |
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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 Amsterdam [u.a.] volume:47 year:2016 pages:71-73 extent:3 |
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High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology |
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Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. |
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Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. |
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Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. |
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High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology |
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