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Study · Animal study (in vivo) · rat · 2026

9 results

Carnosine Potentiates a Compensatory Mitochondrial-Synaptic Proteomic Response in the ALS Cerebellum.

Valerio HP, Oliveira V, Ferreira SY, Pereira IR, Palmisano G, Massafera MP, Bispo VS, Prado FM, Di Mascio P, Medeiros MHG

Antioxidants (Basel, Switzerland)4 Sept 2026

Summary

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive motor neuron degeneration and chronic neuroinflammation in the brain and spinal cord, involving complex interactions between neurons and immune cells. Carnosine (β-alanyl-L-histidine) has pathophysiological relevance due to its ability to detoxify reactive carbonyl species, including α,β-unsaturated aldehydes, scavenge free radicals, and chelate zinc, and has also been proposed to function in the central nervous system as a histidine reservoir for histamine synthesis. Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics. Carnosine treatment extensively remodeled mitochondrial, antioxidant, and synaptic vesicle-trafficking protein networks and increased the abundance of glutamatergic and GABAergic receptor subunits relative to untreated ALS animals, with several of these changes exceeding wild-type levels. Pathway enrichment analyses identified significant up-regulation of Rab-mediated vesicle trafficking, synaptic vesicle cycling, and neurotransmitter transport/secretion pathways, alongside a partial reduction in RNA splicing and proteasomal subunits that were elevated in untreated ALS animals. Cross-comparison with the ALS-associated proteomic signature revealed that most carnosine-responsive proteins followed, rather than reversed, the direction of disease-associated change, indicating that carnosine predominantly potentiates an endogenous compensatory program rather than restoring a wild-type-like proteome. Collectively, these findings show that carnosine drives systems-level remodeling of mitochondrial and synaptic networks in the ALS cerebellum, identifying candidate compensatory pathways and supporting further functional validation of carnosine as a component of multimodal therapeutic strategies in ALS.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In SOD1 G93A ALS rats, carnosine extensively remodeled cerebellar mitochondrial, antioxidant, and synaptic vesicle-trafficking protein networks relative to untreated ALS animals.

    In plain wordsIn SOD1 G93A ALS rats, carnosine extensively remodeled cerebellar mitochondrial, antioxidant, and synaptic vesicle-trafficking protein networks relative to untreated ALS animals.

    Outcome
    Direction not reportedCerebellar protein-network remodeling
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Carnosine treatment extensively remodeled mitochondrial, antioxidant, and synaptic vesicle-trafficking protein networks and increased the abundance of glutamatergic and GABAergic receptor subunits relative to untreated ALS animals, with several of these changes exceeding wild-type levels.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In ALS rats, carnosine increased cerebellar glutamatergic receptor subunit abundance relative to untreated ALS animals.

    In plain wordsIn rats with ALS, carnosine increased cerebellar glutamatergic receptor subunits compared with untreated ALS rats.

    Outcome
    IncreaseGlutamatergic receptor subunits
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Carnosine treatment extensively remodeled mitochondrial, antioxidant, and synaptic vesicle-trafficking protein networks and increased the abundance of glutamatergic and GABAergic receptor subunits relative to untreated ALS animals, with several of these changes exceeding wild-type levels.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In ALS rats, carnosine increased cerebellar GABAergic receptor subunit abundance relative to untreated ALS animals.

    In plain wordsIn rats with ALS, carnosine increased cerebellar GABAergic receptor subunits compared with untreated ALS rats.

    Outcome
    IncreaseGABAergic receptor subunits
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Carnosine treatment extensively remodeled mitochondrial, antioxidant, and synaptic vesicle-trafficking protein networks and increased the abundance of glutamatergic and GABAergic receptor subunits relative to untreated ALS animals, with several of these changes exceeding wild-type levels.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In ALS rats, carnosine significantly increased Rab-mediated vesicle-trafficking pathways.

    In plain wordsIn rats with ALS, carnosine increased Rab-mediated vesicle-trafficking pathways compared with untreated ALS rats.

    Outcome
    IncreaseRab-mediated vesicle trafficking
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pathway enrichment analyses identified significant up-regulation of Rab-mediated vesicle trafficking, synaptic vesicle cycling, and neurotransmitter transport/secretion pathways, alongside a partial reduction in RNA splicing and proteasomal subunits that were elevated in untreated ALS animals.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In ALS rats, carnosine significantly increased synaptic vesicle cycling pathways.

    In plain wordsIn rats with ALS, carnosine increased synaptic vesicle cycling pathways compared with untreated ALS rats.

    Outcome
    IncreaseSynaptic vesicle cycling
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pathway enrichment analyses identified significant up-regulation of Rab-mediated vesicle trafficking, synaptic vesicle cycling, and neurotransmitter transport/secretion pathways, alongside a partial reduction in RNA splicing and proteasomal subunits that were elevated in untreated ALS animals.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In ALS rats, carnosine significantly increased neurotransmitter transport/secretion pathways.

    In plain wordsIn rats with ALS, carnosine increased neurotransmitter transport/secretion pathways compared with untreated ALS rats.

    Outcome
    IncreaseNeurotransmitter transport/secretion
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pathway enrichment analyses identified significant up-regulation of Rab-mediated vesicle trafficking, synaptic vesicle cycling, and neurotransmitter transport/secretion pathways, alongside a partial reduction in RNA splicing and proteasomal subunits that were elevated in untreated ALS animals.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In ALS rats, carnosine partially reduced RNA splicing subunits elevated in untreated ALS animals.

    In plain wordsIn rats with ALS, carnosine partly reduced RNA splicing subunits compared with untreated ALS rats.

    Outcome
    DecreaseRNA splicing subunits
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pathway enrichment analyses identified significant up-regulation of Rab-mediated vesicle trafficking, synaptic vesicle cycling, and neurotransmitter transport/secretion pathways, alongside a partial reduction in RNA splicing and proteasomal subunits that were elevated in untreated ALS animals.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In ALS rats, carnosine partially reduced proteasomal subunits elevated in untreated ALS animals.

    In plain wordsIn rats with ALS, carnosine partly reduced proteasomal subunits compared with untreated ALS rats.

    Outcome
    DecreaseProteasomal subunits
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pathway enrichment analyses identified significant up-regulation of Rab-mediated vesicle trafficking, synaptic vesicle cycling, and neurotransmitter transport/secretion pathways, alongside a partial reduction in RNA splicing and proteasomal subunits that were elevated in untreated ALS animals.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In ALS rats, most carnosine-responsive proteins followed rather than reversed disease-associated changes.

    In plain wordsIn rats with ALS, most proteins affected by carnosine followed rather than reversed disease-associated changes.

    Outcome
    MixedProteomic signature direction
    Study

    ratn: not reported in source

    SOD1 G93A ALS
    Comparator
    Untreated ALS animals
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Cross-comparison with the ALS-associated proteomic signature revealed that most carnosine-responsive proteins followed, rather than reversed, the direction of disease-associated change, indicating that carnosine predominantly potentiates an endogenous compensatory program rather than restoring a wild-type-like proteome.
    1 context sentence
    Summary · context
    Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1G93A ALS rats using quantitative proteomics.

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

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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