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Study · Animal study (in vivo) · mouse · 2014

7 results

Neuroprotective effects of the amylin analogue pramlintide on Alzheimer's disease pathogenesis and cognition.

Adler BL, Yarchoan M, Hwang HM, Louneva N, Blair JA, Palm R, Smith MA, Lee HG, Arnold SE, Casadesus G

Neurobiology of aging11 Oct 2013Cited by 106 (Europe PMC)

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 study7

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In senescence-accelerated prone mice, pramlintide improved novel object recognition performance.

    In plain wordsIn mice, pramlintide improved performance in a test of recognition memory.

    Outcome
    IncreaseNovel object recognition
    Study

    mousen: not reported in source

    Senescence-accelerated prone mouse
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated · infusion · chronicAs given in this study (mouse).

    Source sentences

    Summary
    Pramlintide administration improved performance in the novel object recognition task, a validated test of memory and cognition.
    1 context sentence
    Summary · context
    To investigate mechanisms underlying amylin's effects in the brain, we administered chronic infusions of the amylin analog pramlintide in the senescence-accelerated prone mouse, a mouse model of sporadic AD.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In senescence-accelerated prone mice, pramlintide increased hippocampal synapsin I expression.

    In plain wordsIn mice, pramlintide increased the synaptic marker synapsin I in the hippocampus.

    Outcome
    IncreaseHippocampal synapsin I expression
    Study

    mousen: not reported in source

    Senescence-accelerated prone mouse
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · infusion · chronicAs given in this study (mouse).

    Source sentences

    Summary
    The pramlintide-treated mice had increased expression of the synaptic marker synapsin I and the kinase cyclin-dependent kinase-5 in the hippocampus, as well as decreased oxidative stress and inflammatory markers in the hippocampus.
    1 context sentence
    Summary · context
    To investigate mechanisms underlying amylin's effects in the brain, we administered chronic infusions of the amylin analog pramlintide in the senescence-accelerated prone mouse, a mouse model of sporadic AD.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In senescence-accelerated prone mice, pramlintide increased hippocampal cyclin-dependent kinase-5 expression.

    In plain wordsIn mice, pramlintide increased cyclin-dependent kinase-5 in the hippocampus.

    Outcome
    IncreaseHippocampal cyclin-dependent kinase-5 expression
    Study

    mousen: not reported in source

    Senescence-accelerated prone mouse
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · infusion · chronicAs given in this study (mouse).

    Source sentences

    Summary
    The pramlintide-treated mice had increased expression of the synaptic marker synapsin I and the kinase cyclin-dependent kinase-5 in the hippocampus, as well as decreased oxidative stress and inflammatory markers in the hippocampus.
    1 context sentence
    Summary · context
    To investigate mechanisms underlying amylin's effects in the brain, we administered chronic infusions of the amylin analog pramlintide in the senescence-accelerated prone mouse, a mouse model of sporadic AD.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In senescence-accelerated prone mice, pramlintide decreased hippocampal oxidative stress.

    In plain wordsIn mice, pramlintide decreased oxidative stress in the hippocampus.

    Outcome
    DecreaseHippocampal oxidative stress
    Study

    mousen: not reported in source

    Senescence-accelerated prone mouse
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · infusion · chronicAs given in this study (mouse).

    Source sentences

    Summary
    The pramlintide-treated mice had increased expression of the synaptic marker synapsin I and the kinase cyclin-dependent kinase-5 in the hippocampus, as well as decreased oxidative stress and inflammatory markers in the hippocampus.
    1 context sentence
    Summary · context
    To investigate mechanisms underlying amylin's effects in the brain, we administered chronic infusions of the amylin analog pramlintide in the senescence-accelerated prone mouse, a mouse model of sporadic AD.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In senescence-accelerated prone mice, pramlintide decreased hippocampal inflammatory markers.

    In plain wordsIn mice, pramlintide decreased inflammatory markers in the hippocampus.

    Outcome
    DecreaseHippocampal inflammatory markers
    Study

    mousen: not reported in source

    Senescence-accelerated prone mouse
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · infusion · chronicAs given in this study (mouse).

    Source sentences

    Summary
    The pramlintide-treated mice had increased expression of the synaptic marker synapsin I and the kinase cyclin-dependent kinase-5 in the hippocampus, as well as decreased oxidative stress and inflammatory markers in the hippocampus.
    1 context sentence
    Summary · context
    To investigate mechanisms underlying amylin's effects in the brain, we administered chronic infusions of the amylin analog pramlintide in the senescence-accelerated prone mouse, a mouse model of sporadic AD.
  6. 06LabIn vitro (cells)Mechanism

    In neurons in vitro, pramlintide increased cyclin-dependent kinase-5 in a dose-dependent manner.

    In plain wordsIn cells, pramlintide increased cyclin-dependent kinase-5 as the dose increased.

    Outcome
    IncreaseCyclin-dependent kinase-5
    Study

    n: not reported in source

    Neurons in vitro
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A dose-dependent increase in cyclin-dependent kinase-5 and activation of extracellular-signal-regulated-kinases 1/2 by pramlintide treatment in vitro was also present indicating functionality of the amylin receptor in neurons.
  7. 07LabIn vitro (cells)Mechanism

    In neurons in vitro, pramlintide activated extracellular-signal-regulated kinases.

    In plain wordsIn cells, pramlintide activated extracellular-signal-regulated kinases.

    Outcome
    IncreaseERK activation
    Study

    n: not reported in source

    Neurons in vitro
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A dose-dependent increase in cyclin-dependent kinase-5 and activation of extracellular-signal-regulated-kinases 1/2 by pramlintide treatment in vitro was also present indicating functionality of the amylin receptor in neurons.

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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