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Study · Animal study (in vivo) · mouse · 2019

6 results

Neuroprotective Effects of the Amylin Analog, Pramlintide, on Alzheimer's Disease Are Associated with Oxidative Stress Regulation Mechanisms.

Patrick S, Corrigan R, Grizzanti J, Mey M, Blair J, Pallas M, Camins A, Lee HG, Casadesus G

Journal of Alzheimer's disease : JAD1 Jan 2019Cited by 22 (Europe PMC)

PMID30958347 (opens in a new tab)PMCIDPMC6584632 (opens in a new tab)DOI10.3233/jad-180421 (opens in a new tab)PepBankPUB-30958347
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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

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In APP/PS1 transgenic mice, pramlintide improved cognitive function.

    In plain wordsIn mice, pramlintide improved cognitive function.

    Peptide
    Pramlintide (Symlin)
    Outcome
    IncreaseCognitive function
    Study

    mousen: not reported in source

    APP/PS1 transgenic mice
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    Our data show that Pramlintide improved cognitive function, altered amyloid-processing enzymes, reduced plaque burden in the hippocampus, and regulated endogenous antioxidant enzymes (MnSOD and GPx1) and the stress marker HO-1 in a location specific manner.
    1 context sentence
    Summary · context
    To address this, we treated APP/PS1 transgenic mice with Pramlintide for 3 months, starting at 5.5 months prior to widespread AD pathology onset, and measured cognition (Morris Water Maze), AD pathology, and oxidative stress-related markers and enzymes in vivo.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In APP/PS1 transgenic mice, pramlintide altered amyloid-processing enzymes.

    In plain wordsIn mice, pramlintide changed enzymes involved in amyloid processing.

    Peptide
    Pramlintide (Symlin)
    Outcome
    Direction not reportedAmyloid-processing enzymes
    Study

    mousen: not reported in source

    APP/PS1 transgenic mice
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    Our data show that Pramlintide improved cognitive function, altered amyloid-processing enzymes, reduced plaque burden in the hippocampus, and regulated endogenous antioxidant enzymes (MnSOD and GPx1) and the stress marker HO-1 in a location specific manner.
    1 context sentence
    Summary · context
    To address this, we treated APP/PS1 transgenic mice with Pramlintide for 3 months, starting at 5.5 months prior to widespread AD pathology onset, and measured cognition (Morris Water Maze), AD pathology, and oxidative stress-related markers and enzymes in vivo.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In APP/PS1 transgenic mice, pramlintide reduced plaque burden in the hippocampus.

    In plain wordsIn mice, pramlintide reduced plaque burden in the hippocampus.

    Peptide
    Pramlintide (Symlin)
    Outcome
    DecreaseHippocampal plaque burden
    Study

    mousen: not reported in source

    APP/PS1 transgenic mice
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    Our data show that Pramlintide improved cognitive function, altered amyloid-processing enzymes, reduced plaque burden in the hippocampus, and regulated endogenous antioxidant enzymes (MnSOD and GPx1) and the stress marker HO-1 in a location specific manner.
    1 context sentence
    Summary · context
    To address this, we treated APP/PS1 transgenic mice with Pramlintide for 3 months, starting at 5.5 months prior to widespread AD pathology onset, and measured cognition (Morris Water Maze), AD pathology, and oxidative stress-related markers and enzymes in vivo.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In APP/PS1 transgenic mice, pramlintide regulated endogenous antioxidant enzymes MnSOD and GPx1 and stress marker HO-1 in a location-specific manner.

    In plain wordsIn mice, pramlintide changed antioxidant enzymes MnSOD and GPx1 and stress marker HO-1 in ways that depended on location.

    Peptide
    Pramlintide (Symlin)
    Outcome
    Direction not reportedAntioxidant enzymes and HO-1 regulation
    Study

    mousen: not reported in source

    APP/PS1 transgenic mice
    Outcome group
    Oxidative stress · Nervous system and cognition
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    Our data show that Pramlintide improved cognitive function, altered amyloid-processing enzymes, reduced plaque burden in the hippocampus, and regulated endogenous antioxidant enzymes (MnSOD and GPx1) and the stress marker HO-1 in a location specific manner.
    1 context sentence
    Summary · context
    To address this, we treated APP/PS1 transgenic mice with Pramlintide for 3 months, starting at 5.5 months prior to widespread AD pathology onset, and measured cognition (Morris Water Maze), AD pathology, and oxidative stress-related markers and enzymes in vivo.
  5. 05LabIn vitro (cells)Mechanism

    In neuronal models, pramlintide reduced H2O2-induced endogenous ROS production in a dose-dependent manner.

    In plain wordsIn cells, pramlintide reduced H2O2-induced production of reactive oxygen species in a dose-dependent manner.

    Peptide
    Pramlintide (Symlin)
    Outcome
    DecreaseEndogenous ROS production
    Study

    n: not reported in source

    Neuronal models exposed to H2O2
    Outcome group
    Oxidative stress · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro, Pramlintide treatment in neuronal models reduced H2O2-induced endogenous ROS production and lipid peroxidation in a dose-dependent manner.
  6. 06LabIn vitro (cells)Mechanism

    In neuronal models, pramlintide reduced H2O2-induced lipid peroxidation in a dose-dependent manner.

    In plain wordsIn cells, pramlintide reduced H2O2-induced lipid oxidation in a dose-dependent manner.

    Peptide
    Pramlintide (Symlin)
    Outcome
    DecreaseLipid peroxidation
    Study

    n: not reported in source

    Neuronal models exposed to H2O2
    Outcome group
    Oxidative stress · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro, Pramlintide treatment in neuronal models reduced H2O2-induced endogenous ROS production and lipid peroxidation in a dose-dependent manner.

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

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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