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Oligomeric and fibrillar species of β-amyloid(Aβ42) both impair mitochondrial function in P301L tau transgenic mice

世界最新医学信息文摘 2015年第A期 8-8页

作者： Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Dr?se Ulrich Brandt Marcus F?ndrich Walter E.Müller Jürgen G?tz

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.

关键词： Alzheimer’s disease Amyloid aggregates Amyloid β-peptide Amyloid toxicity Fibrils Frontotemporal dementia globulomer Mitochondria oligomer Protein aggregation respiration tau transgenic mice

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Oligomeric and fibrillar species of β-amyloid(Aβ42) both impair mitochondrial function in P301L tau transgenic mice

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世界最新医学信息文摘 2016年第4期 8-8页

作者： Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drse Ulrich Brandt Marcus Fndrich Walter E.Müller Jiirgen Gtz

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 *** we addressed the role of Aβ,this indicated a synergistic action of tau and Aβpathology on the *** 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 ***,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 *** was not observed with cerebellar preparations indicating selective vulnerability of cortical ***,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 Aβ***,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.

关键词： Alzheimer’s disease Amyloid aggregates Amyloid β-peptide Amyloid toxicity Fibrils Frontotemporal dementia globulomer Mitochondria Oligomer Protein aggregation Respiration Tau Transgenic mice

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Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301L tau transgenic mice

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世界最新医学信息文摘 2015年第99期 1-1页

作者： Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Dr?se Ulrich Brandt Marcus F?ndrich Walter E.Müller Jürgen G?tz

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.

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