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Study · Animal study (in vivo) · rat · 2017

5 results

Lixisenatide attenuates the detrimental effects of amyloid β protein on spatial working memory and hippocampal neurons in rats.

Cai HY, Wang ZJ, Hölscher C, Yuan L, Zhang J, Sun P, Li J, Yang W, Wu MN, Qi JS

Behavioural brain research21 Oct 2016Cited by 37 (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 study5

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In rats, lixisenatide alleviated amyloid β25-35-induced working memory impairment.

    In plain wordsIn rats, lixisenatide reduced amyloid-induced working memory problems compared with the amyloid challenge without lixisenatide.

    Outcome
    DecreaseSpatial working memory impairment
    Study

    ratn: not reported in source

    Amyloid β25-35-induced impairment
    Comparator
    Amyloid β25-35 challenge without lixisenatide
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The results show that lixisenatide effectively alleviated amyloid β protein (Aβ) 25-35-induced working memory impairment,
    1 context sentence
    Summary · context
    Here, we describe additional key neuroprotective properties of lixisenatide and its possible molecular and cellular mechanisms against AD-related impairments in rats.
  2. 02LabIn vitro (cells)Efficacy outcome

    In rat hippocampal cell cultures, lixisenatide reversed amyloid β25-35-triggered cytotoxicity.

    In plain wordsIn cells, lixisenatide reduced amyloid-induced hippocampal cell toxicity compared with the amyloid challenge without lixisenatide.

    Outcome
    DecreaseHippocampal cell cytotoxicity
    Study

    ratn: not reported in source

    Hippocampal cell cultures challenged with Aβ25-35
    Comparator
    Amyloid β25-35 challenge without lixisenatide
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    reversed Aβ25-35-triggered cytotoxicity on hippocampal cell cultures,
    1 context sentence
    Summary · context
    Here, we describe additional key neuroprotective properties of lixisenatide and its possible molecular and cellular mechanisms against AD-related impairments in rats.
  3. 03LabIn vitro (cells)Mechanism

    In the rat hippocampal experimental model, lixisenatide prevented amyloid β25-35-induced Akt-MEK1/2 signaling suppression.

    In plain wordsIn cells, lixisenatide prevented amyloid-induced suppression of the Akt-MEK1/2 pathway compared with the amyloid challenge without lixisenatide.

    Outcome
    DecreaseAkt-MEK1/2 signaling suppression
    Study

    ratn: not reported in source

    Hippocampal cultures with Aβ25-35 challenge
    Comparator
    Amyloid β25-35 challenge without lixisenatide
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and prevented against Aβ25-35-induced suppression of the Akt-MEK1/2 signaling pathway.
  4. 04LabIn vitro (cells)Mechanism

    In the rat hippocampal experimental model, lixisenatide reduced intracellular calcium overload induced by acute amyloid β25-35 application.

    In plain wordsIn cells, lixisenatide reduced amyloid-induced calcium overload compared with the amyloid challenge without lixisenatide.

    Outcome
    DecreaseIntracellular calcium overload
    Study

    ratn: not reported in source

    Hippocampal cultures with Aβ25-35 challenge
    Comparator
    Amyloid β25-35 challenge without lixisenatide
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Lixisenatide also reduced the Aβ25-35 acute application induced intracellular calcium overload, which was abolished by U0126, a specific MEK1/2 inhibitor.

Studies that did not test the peptide alone1

In this study, Lixisenatide was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Lixisenatide.

  1. 05LabNot a test of Lixisenatide aloneIn vitro (cells)Mechanism

    In the rat hippocampal experimental model, U0126 abolished lixisenatide's reduction of amyloid-induced intracellular calcium overload.

    In plain wordsIn cells, lixisenatide's protection against calcium overload disappeared with the MEK1/2 inhibitor U0126 compared with lixisenatide without the inhibitor.

    Outcome
    Direction not reportedMEK1/2 dependence of calcium-overload protection
    Study

    ratn: not reported in source

    Hippocampal cultures with Aβ25-35 challenge
    Comparator
    Lixisenatide without U0126
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    Lixisenatide also reduced the Aβ25-35 acute application induced intracellular calcium overload, which was abolished by U0126, a specific MEK1/2 inhibitor.

    In this study, Lixisenatide was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Lixisenatide.

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

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:36 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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