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Study · Not a test of the peptide alone · 2016

6 results

Mitochondria-targeted molecules MitoQ and SS31 reduce mutant huntingtin-induced mitochondrial toxicity and synaptic damage in Huntington's disease.

Yin X, Manczak M, Reddy PH

Human molecular genetics16 Feb 2016Cited by 121 (Europe PMC)

PMID26908605 (opens in a new tab)PMCIDPMC4986329 (opens in a new tab)DOI10.1093/hmg/ddw045 (opens in a new tab)PepBankPUB-26908605
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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: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone6

In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Elamipretide (SS-31).

  1. 01LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In mutant huntingtin striatal neurons, treatment with MitoQ and SS31 together reported as a pair down-regulated the fission genes Drp1 and Fis1.

    In plain wordsIn lab-grown Huntington's disease neurons, MitoQ and SS31 treatment, reported together, lowered mitochondrial splitting genes.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMitochondrial fission genes Drp1 and Fis1
    Study

    n: not reported in source

    STHDhQ111/Q111 striatal neurons expressing mutant huntingtin
    Comparator
    Untreated mutant Htt neurons
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    In the MitoQ- and SS31-treated mutant Htt neurons, fission genes Drp1 and Fis1 were down-regulated, and fusion genes Mfn1, Mfn2 and Opa1 were up-regulated relative to untreated neurons
    1 context sentence
    Summary · context
    The objective of this study was to determine the protective effects of the mitochondria-targeted molecules MitoQ and SS31 in striatal neurons that stably express mutant huntingtin (Htt) (STHDhQ111/Q111) in Huntington's disease (HD).

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

  2. 02LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In mutant huntingtin striatal neurons, treatment with MitoQ and SS31 together reported as a pair up-regulated the fusion genes Mfn1, Mfn2 and Opa1.

    In plain wordsIn lab-grown Huntington's disease neurons, MitoQ and SS31 treatment, reported together, raised mitochondrial joining genes.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseMitochondrial fusion genes Mfn1, Mfn2 and Opa1
    Study

    n: not reported in source

    STHDhQ111/Q111 striatal neurons expressing mutant huntingtin
    Comparator
    Untreated mutant Htt neurons
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    In the MitoQ- and SS31-treated mutant Htt neurons, fission genes Drp1 and Fis1 were down-regulated, and fusion genes Mfn1, Mfn2 and Opa1 were up-regulated relative to untreated neurons
    1 context sentence
    Summary · context
    The objective of this study was to determine the protective effects of the mitochondria-targeted molecules MitoQ and SS31 in striatal neurons that stably express mutant huntingtin (Htt) (STHDhQ111/Q111) in Huntington's disease (HD).

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

  3. 03LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In mutant huntingtin striatal neurons, MitoQ and SS31 treatment, reported together, up-regulated the mitochondrial biogenesis genes PGC1α, PGC1β, Nrf1, Nrf2 and TFAM.

    In plain wordsIn lab-grown Huntington's disease neurons, MitoQ and SS31 treatment, reported together, raised genes that build new mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseMitochondrial biogenesis genes PGC1α, PGC1β, Nrf1, Nrf2 and TFAM
    Study

    n: not reported in source

    STHDhQ111/Q111 striatal neurons expressing mutant huntingtin
    Comparator
    Untreated mutant Htt neurons
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    Interestingly, the mitochondrial biogenesis genes PGC1α, PGC1β, Nrf1, Nrf2 and TFAM were up-regulated in MitoQ- and SS31-treated mutant Htt neurons.
    1 context sentence
    Summary · context
    The objective of this study was to determine the protective effects of the mitochondria-targeted molecules MitoQ and SS31 in striatal neurons that stably express mutant huntingtin (Htt) (STHDhQ111/Q111) in Huntington's disease (HD).

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

  4. 04LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In mutant huntingtin striatal neurons, MitoQ and SS31 treatment, reported together, up-regulated the synaptic genes synaptophysin and PSD95.

    In plain wordsIn lab-grown Huntington's disease neurons, MitoQ and SS31 treatment, reported together, raised synapse genes.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseSynaptic genes synaptophysin and PSD95
    Study

    n: not reported in source

    STHDhQ111/Q111 striatal neurons expressing mutant huntingtin
    Comparator
    Untreated mutant Htt neurons
    Outcome group
    Neuroprotection · Nervous system and cognition

    Source sentences

    Summary
    The synaptic genes synaptophysin and PSD95 were up-regulated
    1 context sentence
    Summary · context
    The objective of this study was to determine the protective effects of the mitochondria-targeted molecules MitoQ and SS31 in striatal neurons that stably express mutant huntingtin (Htt) (STHDhQ111/Q111) in Huntington's disease (HD).

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

  5. 05LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In mutant huntingtin striatal neurons, mitochondrial function was normal after MitoQ and SS31 treatment, reported together.

    In plain wordsIn lab-grown Huntington's disease neurons, mitochondrial function was normal after MitoQ and SS31 treatment, reported together.

    Peptide
    Elamipretide (SS-31)
    Outcome
    Not applicableMitochondrial function
    Study

    n: not reported in source

    STHDhQ111/Q111 striatal neurons expressing mutant huntingtin
    Comparator
    Untreated mutant Htt neurons
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    and mitochondrial function was normal in the MitoQ- and SS31-treated mutant Htt neurons.
    1 context sentence
    Summary · context
    The objective of this study was to determine the protective effects of the mitochondria-targeted molecules MitoQ and SS31 in striatal neurons that stably express mutant huntingtin (Htt) (STHDhQ111/Q111) in Huntington's disease (HD).

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

  6. 06LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In mutant huntingtin striatal neurons, transmission electron microscopy showed decreased numbers of structurally intact mitochondria after MitoQ and SS31 treatment, reported together.

    In plain wordsIn lab-grown Huntington's disease neurons, MitoQ and SS31 treatment, reported together, was linked to fewer structurally intact mitochondria under the electron microscope.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseStructurally intact mitochondria (TEM)
    Study

    n: not reported in source

    STHDhQ111/Q111 striatal neurons expressing mutant huntingtin
    Comparator
    Untreated mutant Htt neurons
    Outcome group
    Mitochondrial function · Nervous system and cognition

    Source sentences

    Summary
    TEM studies revealed decreased numbers of structurally intact mitochondria in MitoQ- and SS31-treated mutant Htt neurons.
    1 context sentence
    Summary · context
    The objective of this study was to determine the protective effects of the mitochondria-targeted molecules MitoQ and SS31 in striatal neurons that stably express mutant huntingtin (Htt) (STHDhQ111/Q111) in Huntington's disease (HD).

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

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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