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Study · Animal study (in vivo) · mouse · 2023

5 results

Neuroprotective Mechanisms of Amylin Receptor Activation, Not Antagonism, in the APP/PS1 Mouse Model of Alzheimer's Disease.

Corrigan RR, Labrador L, Grizzanti J, Mey M, Piontkivska H, Casadesús G

Journal of Alzheimer's disease : JAD1 Jan 2023Cited by 6 (Europe PMC)

PMID36641678 (opens in a new tab)DOI10.3233/jad-221057 (opens in a new tab)PepBankPUB-36641678
Publisher pagePubMedAsk about this study
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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 study5

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In AD-modeled mice, pramlintide improved cognitive function independently of central receptor activation.

    In plain wordsIn mice with an Alzheimer's disease model, pramlintide improved thinking function independently of central receptor activation.

    Peptide
    Pramlintide (Symlin)
    Outcome
    IncreaseCognitive function
    Study

    mousen: not reported in source

    APP/PS1 Alzheimer's disease model
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    Here we show that pramlintide improved cognitive function independently of CNS receptor activation and provide transcriptomic data that highlights potential mechanisms.
    1 context sentence
    Summary · context
    To address these questions more directly we delivered the amylin analog pramlintide systemically (IP), at previously identified therapeutic doses, while centrally (ICV) inhibiting the receptor using an amylin receptor antagonist (AC187), at doses known to impact CNS function.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In female APP/PS1 mice, peripheral pramlintide mitigated the increased amyloid-beta pathology caused by amylin receptor inhibition.

    In plain wordsIn female APP/PS1 mice, pramlintide reduced the worsening of amyloid-beta pathology caused by receptor inhibition.

    Peptide
    Pramlintide (Symlin)
    Outcome
    DecreaseAmyloid-beta pathology under receptor inhibition
    Study

    mousen: not reported in source

    APP/PS1 Alzheimer's disease model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, we show than inhibition of the amylin receptor increased amyloid-beta pathology in female APP/PS1 mice, an effect than was mitigated by peripheral delivery of pramlintide.
    1 context sentence
    Summary · context
    To address these questions more directly we delivered the amylin analog pramlintide systemically (IP), at previously identified therapeutic doses, while centrally (ICV) inhibiting the receptor using an amylin receptor antagonist (AC187), at doses known to impact CNS function.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In female AD-modeled mice, transcriptomic analysis linked pramlintide therapy to oxidative stress protection.

    In plain wordsIn female mice, gene activity analysis linked pramlintide to oxidative stress protection mechanisms.

    Peptide
    Pramlintide (Symlin)
    Outcome
    Direction not reportedOxidative stress protection in females
    Study

    mousen: not reported in source

    APP/PS1 Alzheimer's disease model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    Through transcriptomic analysis of pramlintide therapy in AD-modeled mice we found sexual dimorphic modulation of neuroprotective mechanisms: oxidative stress protection in females and membrane stability and reduced neuronal excitability markers in males.
    1 context sentence
    Summary · context
    To address these questions more directly we delivered the amylin analog pramlintide systemically (IP), at previously identified therapeutic doses, while centrally (ICV) inhibiting the receptor using an amylin receptor antagonist (AC187), at doses known to impact CNS function.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In male AD-modeled mice, transcriptomic analysis linked pramlintide therapy to membrane stability.

    In plain wordsIn male mice with an Alzheimer's disease model, gene activity analysis linked pramlintide to membrane stability.

    Peptide
    Pramlintide (Symlin)
    Outcome
    Direction not reportedMembrane stability in males
    Study

    mousen: not reported in source

    APP/PS1 Alzheimer's disease model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    Through transcriptomic analysis of pramlintide therapy in AD-modeled mice we found sexual dimorphic modulation of neuroprotective mechanisms: oxidative stress protection in females and membrane stability and reduced neuronal excitability markers in males.
    1 context sentence
    Summary · context
    To address these questions more directly we delivered the amylin analog pramlintide systemically (IP), at previously identified therapeutic doses, while centrally (ICV) inhibiting the receptor using an amylin receptor antagonist (AC187), at doses known to impact CNS function.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In male AD-modeled mice, pramlintide therapy reduced neuronal excitability markers in transcriptomic analysis.

    In plain wordsIn male mice with an Alzheimer's disease model, pramlintide reduced markers of nerve-cell excitability.

    Peptide
    Pramlintide (Symlin)
    Outcome
    DecreaseNeuronal excitability markers in males
    Study

    mousen: not reported in source

    APP/PS1 Alzheimer's disease model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    Through transcriptomic analysis of pramlintide therapy in AD-modeled mice we found sexual dimorphic modulation of neuroprotective mechanisms: oxidative stress protection in females and membrane stability and reduced neuronal excitability markers in males.
    1 context sentence
    Summary · context
    To address these questions more directly we delivered the amylin analog pramlintide systemically (IP), at previously identified therapeutic doses, while centrally (ICV) inhibiting the receptor using an amylin receptor antagonist (AC187), at doses known to impact CNS function.

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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