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Study · In vitro (cells) · mouse · 2010

5 results

Mitochondria-targeted antioxidants protect against amyloid-beta toxicity in Alzheimer's disease neurons.

Manczak M, Mao P, Calkins MJ, Cornea A, Reddy AP, Murphy MP, Szeto HH, Park B, Reddy PH

Journal of Alzheimer's disease : JAD1 Jan 2010Cited by 366 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC. Results still quote short attributed sentences.

Results from this study5

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In mouse N2a cells incubated with amyloid-beta, treatment with MitoQ, SS31 and resveratrol prevented the abnormal expression of peroxiredoxins and mitochondrial structural genes.

    In plain wordsIn cells, treatment with SS31 and two other agents prevented amyloid-beta from disturbing the activity of protective and mitochondrial genes.

    Outcome
    IncreasePeroxiredoxin and mitochondrial structural gene expression
    Study

    mousen: not reported in source

    Mouse neuroblastoma (N2a) cells incubated with amyloid-beta
    Comparator
    Amyloid-beta alone
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    abnormal expression of peroxiredoxins and mitochondrial structural genes were prevented
    1 context sentence
    Summary · context
    Using electron and confocal microscopy, gene expression analysis, and biochemical methods, we studied mitochondrial structure and function and neurite outgrowth in N2a cells treated with MitoQ, SS31, and resveratrol, and then incubated with Abeta.
  2. 02LabIn vitro (cells)Mechanism

    In mouse N2a cells incubated with amyloid-beta, treatment with MitoQ, SS31 and resveratrol kept mitochondrial function normal and mitochondria intact.

    In plain wordsIn cells, treatment with SS31 and two other agents kept mitochondria working normally and intact despite amyloid-beta.

    Outcome
    IncreaseMitochondrial function and structure
    Study

    mousen: not reported in source

    Mouse neuroblastoma (N2a) cells incubated with amyloid-beta
    Comparator
    Amyloid-beta alone
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    mitochondrial function was normal; intact mitochondria were present
    1 context sentence
    Summary · context
    Using electron and confocal microscopy, gene expression analysis, and biochemical methods, we studied mitochondrial structure and function and neurite outgrowth in N2a cells treated with MitoQ, SS31, and resveratrol, and then incubated with Abeta.
  3. 03LabIn vitro (cells)Efficacy outcome

    In mouse N2a cells incubated with amyloid-beta, treatment with MitoQ, SS31 and resveratrol significantly increased neurite outgrowth.

    In plain wordsIn cells, treatment with SS31 and two other agents increased the growth of nerve cell extensions reduced by amyloid-beta.

    Outcome
    IncreaseNeurite outgrowth in N2a cells
    Study

    mousen: not reported in source

    Mouse neuroblastoma (N2a) cells incubated with amyloid-beta
    Comparator
    Amyloid-beta alone
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    neurite outgrowth was significantly increased.
    1 context sentence
    Summary · context
    Using electron and confocal microscopy, gene expression analysis, and biochemical methods, we studied mitochondrial structure and function and neurite outgrowth in N2a cells treated with MitoQ, SS31, and resveratrol, and then incubated with Abeta.
  4. 04LabIn vitro (cells)Efficacy outcome

    In primary neurons from amyloid-beta precursor protein transgenic mice, treatment with MitoQ and SS31 significantly increased neurite outgrowth.

    In plain wordsIn neurons from mice with an Alzheimer's-type gene, treatment with SS31 and MitoQ increased the growth of nerve cell extensions.

    Outcome
    IncreaseNeurite outgrowth in primary neurons
    Study

    mousen: not reported in source

    Primary neurons from amyloid-beta precursor protein transgenic mice
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In primary neurons from amyloid-beta precursor protein transgenic mice that were treated with MitoQ and SS31, neurite outgrowth was significantly increased
  5. 05LabIn vitro (cells)Mechanism

    In primary neurons from amyloid-beta precursor protein transgenic mice, treatment with MitoQ and SS31 significantly decreased cyclophilin D expression.

    In plain wordsIn neurons from mice with an Alzheimer's-type gene, treatment with SS31 and MitoQ lowered levels of cyclophilin D, a mitochondrial protein.

    Outcome
    DecreaseCyclophilin D expression in primary neurons
    Study

    mousen: not reported in source

    Primary neurons from amyloid-beta precursor protein transgenic mice
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    cyclophilin D expression was significantly decreased.
    1 context sentence
    Summary · context
    In primary neurons from amyloid-beta precursor protein transgenic mice that were treated with MitoQ and SS31

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

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