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Study · Animal study (in vivo) · mouse · 2024

3 results

Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer's disease.

Calvo-Rodriguez M, Kharitonova EK, Snyder AC, Hou SS, Sanchez-Mico MV, Das S, Fan Z, Shirani H, Nilsson KPR, Serrano-Pozo A, Bacskai BJ

Molecular neurodegeneration18 Jan 2024Cited by 70 (Europe PMC)

PMID38238819 (opens in a new tab)PMCIDPMC10797952 (opens in a new tab)DOI10.1186/s13024-024-00702-2 (opens in a new tab)PepBankPUB-38238819
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Summary

BackgroundReactive oxidative stress is a critical player in the amyloid beta (Aβ) toxicity that contributes to neurodegeneration in Alzheimer's disease (AD). Damaged mitochondria are one of the main sources of reactive oxygen species and accumulate in Aβ plaque-associated dystrophic neurites in the AD brain. Although Aβ causes neuronal mitochondria reactive oxidative stress in vitro, this has never been directly observed in vivo in the living mouse brain. Here, we tested for the first time whether Aβ plaques and soluble Aβ oligomers induce mitochondrial oxidative stress in surrounding neurons in vivo, and whether this neurotoxic effect can be abrogated using mitochondrial-targeted antioxidants.MethodsWe expressed a genetically encoded fluorescent ratiometric mitochondria-targeted reporter of oxidative stress in mouse models of the disease and performed intravital multiphoton microscopy of neuronal mitochondria and Aβ plaques.ResultsFor the first time, we demonstrated by direct observation in the living mouse brain exacerbated mitochondrial oxidative stress in neurons after both Aβ plaque deposition and direct application of soluble oligomeric Aβ onto the brain, and determined the most likely pathological sequence of events leading to oxidative stress in vivo. Oxidative stress could be inhibited by both blocking calcium influx into mitochondria and treating with the mitochondria-targeted antioxidant SS31. Remarkably, the latter ameliorated plaque-associated dystrophic neurites without impacting Aβ plaque burden.ConclusionsConsidering these results, combination of mitochondria-targeted compounds with other anti-amyloid beta or anti-tau therapies hold promise as neuroprotective drugs for the prevention and/or treatment of AD.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In living mouse brain in Alzheimer's disease models, treatment with the mitochondria-targeted antioxidant SS31 inhibited mitochondrial oxidative stress.

    In plain wordsIn mice with Alzheimer's-like disease, SS31 lowered oxidative stress in nerve-cell mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMitochondrial oxidative stress
    Study

    mousen: not reported in source

    Mouse models of Alzheimer's disease (intravital imaging)
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Oxidative stress could be inhibited by both blocking calcium influx into mitochondria and treating with the mitochondria-targeted antioxidant SS31.
    1 context sentence
    Summary · context
    We expressed a genetically encoded fluorescent ratiometric mitochondria-targeted reporter of oxidative stress in mouse models of the disease and performed intravital multiphoton microscopy of neuronal mitochondria and Aβ plaques.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mouse models of Alzheimer's disease, SS31 ameliorated plaque-associated dystrophic neurites.

    In plain wordsIn mice with Alzheimer's-like disease, SS31 reduced damage to nerve fibres near amyloid plaques.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreasePlaque-associated dystrophic neurites
    Study

    mousen: not reported in source

    Mouse models of Alzheimer's disease (intravital imaging)
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Remarkably, the latter ameliorated plaque-associated dystrophic neurites without impacting Aβ plaque burden.
    1 context sentence
    Summary · context
    We expressed a genetically encoded fluorescent ratiometric mitochondria-targeted reporter of oxidative stress in mouse models of the disease and performed intravital multiphoton microscopy of neuronal mitochondria and Aβ plaques.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mouse models of Alzheimer's disease, SS31 did not change Abeta plaque burden.

    In plain wordsIn mice with Alzheimer's-like disease, SS31 did not change the amount of amyloid plaque.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeAbeta plaque burden
    Study

    mousen: not reported in source

    Mouse models of Alzheimer's disease (intravital imaging)
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Remarkably, the latter ameliorated plaque-associated dystrophic neurites without impacting Aβ plaque burden.
    1 context sentence
    Summary · context
    We expressed a genetically encoded fluorescent ratiometric mitochondria-targeted reporter of oxidative stress in mouse models of the disease and performed intravital multiphoton microscopy of neuronal mitochondria and Aβ plaques.

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

Terms as the source lists them.

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