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Study · Animal study (in vivo) · mouse · 2025

2 results

The Potential of the Peptide Drug Semax and Its Derivative for Correcting Pathological Impairments in the Animal Model of Alzheimer's Disease.

Radchenko AI, Kuzubova EV, Apostol AA, Mitkevich VA, Andreeva LA, Limborska SA, Stepenko YV, Shmigerova VS, Solin AV, Korokin MV, Pokrovskii MV, Myasoedov NF, Makarov AA

Acta naturae1 Oct 2025Cited by 1 (Europe PMC)

PMID41479572 (opens in a new tab)PMCIDPMC12755871 (opens in a new tab)DOI10.32607/actanaturae.27808 (opens in a new tab)PepBankPUB-41479572
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Summary

Alzheimer's disease, first described over a century ago, is currently among the most common neurodegenerative diseases whose significance is increasingly growing with the aging of populations. Throughout the entire period of its study, no remedies have been found that would be effective in treating - or at least significantly slowing - the pathological process, while being sufficiently safe. In this regard, significant attention is paid to the development and application of natural peptide drugs lacking side effects. The present study assessed the effect of the known neuroprotective peptide Semax and its derivative on the behavioral characteristics and development of amyloidosis in transgenic APPswe/PS1dE9/Blg mice acting as a model of Alzheimer's disease. The open field, novel object recognition, and Barnes maze tests demonstrated that both Semax and its derivative improved cognitive functions in mice. Histological examination showed that these peptides reduced the number of amyloid inclusions in the cortex and hippocampus of the animals' brains. These findings demonstrate the high potential of Semax and its derivatives when used to develop therapeutic and corrective strategies for Alzheimer's disease.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In transgenic Alzheimer's disease model mice, Semax and its derivative improved cognitive function in the open field, novel object recognition and Barnes maze tests.

    In plain wordsIn mice with an Alzheimer's-like disease, Semax and its derivative improved performance in memory and behavior tests.

    Peptide
    Semax
    Outcome
    IncreaseCognitive function (open field, novel object recognition, Barnes maze)
    Study

    mousen: not reported in source

    APPswe/PS1dE9/Blg transgenic mice (Alzheimer's disease model)
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The open field, novel object recognition, and Barnes maze tests demonstrated that both Semax and its derivative improved cognitive functions in mice.
    1 context sentence
    Summary · context
    The present study assessed the effect of the known neuroprotective peptide Semax and its derivative on the behavioral characteristics and development of amyloidosis in transgenic APPswe/PS1dE9/Blg mice acting as a model of Alzheimer's disease.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In transgenic Alzheimer's disease model mice, Semax and its derivative reduced the number of amyloid inclusions in the cortex and hippocampus.

    In plain wordsIn mice with an Alzheimer's-like disease, Semax and its derivative lowered the number of amyloid deposits in the brain.

    Peptide
    Semax
    Outcome
    DecreaseAmyloid inclusions in cortex and hippocampus
    Study

    mousen: not reported in source

    APPswe/PS1dE9/Blg transgenic mice (Alzheimer's disease model)
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    these peptides reduced the number of amyloid inclusions in the cortex and hippocampus of the animals' brains.
    1 context sentence
    Summary · context
    The present study assessed the effect of the known neuroprotective peptide Semax and its derivative on the behavioral characteristics and development of amyloidosis in transgenic APPswe/PS1dE9/Blg mice acting as a model of Alzheimer's disease.

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, 10:21 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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