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| 1 | Mitochondrial dysfunction in sporadic and genetic Alzheimer’s disease显示文摘 | Susanne Hauptmann Uta Keil Isabel Scherping Astrid Bonert Anne Eckert Walter E. Müller | 2006 | Experimental Gerontology2006，，： | 1 |
| 2 | Oligomeric and fibrillar species of β-amyloid(Aβ42) both impair mitochondrial function in P301L tau transgenic mice显示文摘We recently provided evidence for a mitochondrial dysfunction in P301L tau transgenic mice,a strain modeling the tau pathology of Alzheimer's disease(AD)and frontotemporal dementia(FTD).In addition to tau aggregates,the AD brain is further characterized by Aβpeptide-containing plaques.When we addressed the role of Aβ,this indicated a synergistic action of tau and Aβpathology on the mitochondria.In the present study,we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβmight be the actual toxic species.Interestingly,both oligomeric and fibrillar,but not disaggregated(mainly monomeric)Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301L tau transgenic mice.This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons.Furthermore,we found reductions in state 3 respiration,the respiratory control ratio,and uncoupled respiration when incubating P301L tau mitochondria either with oligomeric or fibrillar preparations of Aβ42.Finally,we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic,but exert different degrees of toxicity. | Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drse Ulrich Brandt Marcus Fndrich Walter E.Müller Jiirgen Gtz | 2016 | 世界最新医学信息文摘2016，16，2： | 1 |
| 3 | Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301L tau transgenic mice显示文摘We recently provided evidence for a mitochondrial dysfunction in P301L tau transgenic mice, a strain modeling the tau pathology of alzheimer's disease(ad) and frontotemporal dementia(ftd). in addition to tau aggregates, the ad brain is further characterized by Aβ peptide-containing plaques. When we addressed the role of Aβ, this indicated a synergistic action of tau and Aβ pathology on the mitochondria. In the present study, we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβ might be the actual toxic species. Interestingly, both oligomeric and fibrillar, but not disaggregated(mainly monomeric) Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301L tau transgenic mice. This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons. Furthermore, we found reductions in state 3 respiration, the respiratory control ratio, and uncoupled respiration when incubating P301L tau mitochondria either with oligomeric or fibrillar preparations of Aβ42. Finally, we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic, but exert different degrees of toxicity. | Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz | 2015 | 世界最新医学信息文摘2015，15，99： | 0 |
| 4 | Oligomeric and fibrillar species ofβ-amyloid(A β 42)both impair mitochondrial function in P301L tau transgenic mice显示文摘We recently provided evidence for a mitochondrial dysfunction in P301 l tau transgenic mice, a strain modeling the tau pathology of alzheimer's disease(ad) and frontotemporal dementia(ftd). in addition to tau aggregates, the ad brain is further characterized by Aβ peptide-containing plaques. When we addressed the role of Aβ, this indicated a synergistic action of tau and Aβ pathology on the mitochondria. In the present study, we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβ might be the actual toxic species. Interestingly, both oligomeric and fibrillar, but not disaggregated(mainly monomeric) Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301 L tau transgenic mice. This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons. Furthermore, we found reductions in state 3 respiration, the respiratory control ratio, and uncoupled respiration when incubating P301 L tau mitochondria either with oligomeric or fibrillar preparations of Aβ42. Finally, we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic, but exert different degrees of toxicity. | Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz | 2015 | 世界最新医学信息文摘2015，15，A0： | 0 |
| 5 | Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301L tau transgenic mice显示文摘We recently provided evidence for a mitochondrial dysfunction in P301 l tau transgenic mice, a strain modeling the tau pathology of alzheimer's disease(ad) and frontotemporal dementia(ftd). in addition to tau aggregates, the ad brain is further characterized by Aβ peptide-containing plaques. When we addressed the role of Aβ, this indicated a synergistic action of tau and Aβ pathology on the mitochondria. In the present study, we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβ might be the actual toxic species. Interestingly, both oligomeric and fibrillar, but not disaggregated(mainly monomeric) Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301 L tau transgenic mice. This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons. Furthermore, we found reductions in state 3 respiration, the respiratory control ratio, and uncoupled respiration when incubating P301 L tau mitochondria either with oligomeric or fibrillar preparations of Aβ42. Finally, we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic, but exert different degrees of toxicity. | Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz | 2015 | 世界最新医学信息文摘2015，15，90： | 0 |
| 6 | Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301L tau transgenic mice显示文摘We recently provided evidence for a mitochondrial dysfunction in P301 L tau transgenic mice,a strain modeling the tau pathology of Alzheimer's disease(AD) and frontotemporal dementia(FTD).In addition to tau aggregates,the AD brain is further characterized by Aβ peptide-containing plaques.When we addressed the role of Aβ,this indicated a synergistic action of tau and Aβ pathology on the mitochondria.In the present study,we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβ might be the actual toxic species.Interestingly,both oligomeric and fibrillar,but not disaggregated(mainly monomeric) Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301 L tau transgenic mice.This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons.Furthermore,we found reductions in state 3 respiration,the respiratory control ratio,and uncoupled respiration when incubating P301 L tau mitochondria either with oligomeric or fibrillar preparations of Aβ42.Finally,we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic,but exert different degrees of toxicity. | Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz | 2016 | 世界最新医学信息文摘2016，16，4： | 0 |
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