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Study · Animal study (in vivo) · rat · 2021

9 results

Neuroprotection of Exendin-4 by Enhanced Autophagy in a Parkinsonian Rat Model of α-Synucleinopathy.

Bu LL, Liu YQ, Shen Y, Fan Y, Yu WB, Jiang DL, Tang YL, Yang YJ, Wu P, Zuo CT, Koprich JB, Liu FT, Wu JJ, Wang J

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics15 Mar 2021Cited by 47 (Europe PMC)

PMID33723752 (opens in a new tab)PMCIDPMC8423983 (opens in a new tab)DOI10.1007/s13311-021-01018-5 (opens in a new tab)PepBankPUB-33723752
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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 study9

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In parkinsonian rats, exendin‑4 attenuated tyrosine-hydroxylase-positive neuronal loss.

    In plain wordsIn rats with a Parkinson's disease model, exendin‑4 reduced loss of dopamine-related neurons.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseTyrosine-hydroxylase-positive neuronal loss
    Study

    ratn: not reported in source

    AAV-9-A53T-alpha-synuclein parkinsonian model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    5 μg/kg/day · intraperitoneal · 4 or 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Positron emission tomography/computed tomography (PET/CT) scanning and immunostaining established that treatment with exendin-4 attenuated tyrosine-hydroxylase-positive neuronal loss and terminal denervation and mitigated the decrease in expression of vesicular monoamine transporter 2 within the nig…
    1 context sentence
    Summary · context
    This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In parkinsonian rats, exendin‑4 attenuated terminal denervation.

    In plain wordsIn rats with a Parkinson's disease model, exendin‑4 reduced loss of nerve terminals.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseTerminal denervation
    Study

    ratn: not reported in source

    AAV-9-A53T-alpha-synuclein parkinsonian model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    5 μg/kg/day · intraperitoneal · 4 or 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Positron emission tomography/computed tomography (PET/CT) scanning and immunostaining established that treatment with exendin-4 attenuated tyrosine-hydroxylase-positive neuronal loss and terminal denervation and mitigated the decrease in expression of vesicular monoamine transporter 2 within the nig…
    1 context sentence
    Summary · context
    This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In parkinsonian rats, exendin‑4 mitigated reduced vesicular monoamine transporter 2 expression in the nigrostriatal dopaminergic system.

    In plain wordsIn rats with a Parkinson's disease model, exendin‑4 limited the loss of a transporter in dopamine pathways.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseVesicular monoamine transporter 2 expression
    Study

    ratn: not reported in source

    AAV-9-A53T-alpha-synuclein parkinsonian model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    5 μg/kg/day · intraperitoneal · 4 or 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Positron emission tomography/computed tomography (PET/CT) scanning and immunostaining established that treatment with exendin-4 attenuated tyrosine-hydroxylase-positive neuronal loss and terminal denervation and mitigated the decrease in expression of vesicular monoamine transporter 2 within the nig…
    1 context sentence
    Summary · context
    This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In parkinsonian rats, exendin‑4 mitigated motor deficits in behavioral tests.

    In plain wordsIn rats with a Parkinson's disease model, exendin‑4 reduced movement problems.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseMotor deficits
    Study

    ratn: not reported in source

    AAV-9-A53T-alpha-synuclein parkinsonian model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    5 μg/kg/day · intraperitoneal · 4 or 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    It also mitigated the parkinsonian motor deficits assessed in behavioral tests.
    1 context sentence
    Summary · context
    This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In parkinsonian rats, exendin‑4 promoted autophagy, with effects counteracted by autophagy inhibitors.

    In plain wordsIn rats with a Parkinson's disease model, exendin‑4 increased cellular recycling, with effects blocked by autophagy inhibitors.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseAutophagy
    Study

    ratn: not reported in source

    AAV-9-A53T-alpha-synuclein parkinsonian model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    5 μg/kg/day · intraperitoneal · 4 or 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Furthermore, through both in vivo and in vitro models of Parkinson's disease, we showed that exendin-4 promoted autophagy and mediated degradation of pathological α-synuclein, the effects of which were counteracted by 3-methyladenine or chloroquine, the autophagic inhibitors.
    1 context sentence
    Summary · context
    This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In parkinsonian rats, exendin‑4 promoted pathological alpha-synuclein degradation, with effects counteracted by autophagy inhibitors.

    In plain wordsIn rats with a Parkinson's disease model, exendin‑4 increased abnormal protein breakdown, with effects blocked by autophagy inhibitors.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreasePathological alpha-synuclein degradation
    Study

    ratn: not reported in source

    AAV-9-A53T-alpha-synuclein parkinsonian model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    5 μg/kg/day · intraperitoneal · 4 or 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Furthermore, through both in vivo and in vitro models of Parkinson's disease, we showed that exendin-4 promoted autophagy and mediated degradation of pathological α-synuclein, the effects of which were counteracted by 3-methyladenine or chloroquine, the autophagic inhibitors.
    1 context sentence
    Summary · context
    This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In parkinsonian rats, exendin‑4 attenuated PI3K/Akt/mTOR pathway dysregulation.

    In plain wordsIn rats with a Parkinson's disease model, exendin‑4 reduced disruption of the PI3K/Akt/mTOR pathway.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreasePI3K/Akt/mTOR pathway dysregulation
    Study

    ratn: not reported in source

    AAV-9-A53T-alpha-synuclein parkinsonian model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    5 μg/kg/day · intraperitoneal · 4 or 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Additionally, exendin-4 attenuated dysregulation of the PI3K/Akt/mTOR pathway in rats injected with AAV-9-A53T-α-synuclein.
    1 context sentence
    Summary · context
    This model was established by unilaterally injecting AAV-9-A53T-α-synuclein into the right substantia nigra pars compacta, followed by 4 or 8 weeks of twice-daily intraperitoneal injections of exendin-4 (5 μg/kg/day) starting at 2 weeks after AAV-9-A53T-α-synuclein injections.
  8. 08LabIn vitro (cells)Mechanism

    In an in vitro Parkinson's disease model, exendin‑4 promoted autophagy, with effects counteracted by autophagy inhibitors.

    In plain wordsIn lab models of Parkinson's disease, exendin‑4 increased cellular recycling, with effects blocked by autophagy inhibitors.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseAutophagy in vitro
    Study

    n: not reported in source

    In vitro Parkinson's disease model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, through both in vivo and in vitro models of Parkinson's disease, we showed that exendin-4 promoted autophagy and mediated degradation of pathological α-synuclein, the effects of which were counteracted by 3-methyladenine or chloroquine, the autophagic inhibitors.
  9. 09LabIn vitro (cells)Mechanism

    In an in vitro Parkinson's disease model, exendin‑4 promoted pathological alpha-synuclein degradation, with effects counteracted by autophagy inhibitors.

    In plain wordsIn lab models of Parkinson's disease, exendin‑4 increased abnormal protein breakdown, with effects blocked by autophagy inhibitors.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreasePathological alpha-synuclein degradation in vitro
    Study

    n: not reported in source

    In vitro Parkinson's disease model
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, through both in vivo and in vitro models of Parkinson's disease, we showed that exendin-4 promoted autophagy and mediated degradation of pathological α-synuclein, the effects of which were counteracted by 3-methyladenine or chloroquine, the autophagic inhibitors.

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

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