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Study · In vitro (cells) · 2017

1 result

Impairment of mitochondria dynamics by human A53T α-synuclein and rescue by NAP (davunetide) in a cell model for Parkinson's disease.

Melo TQ, van Zomeren KC, Ferrari MF, Boddeke HW, Copray JC

Experimental brain research19 Nov 2016Cited by 29 (Europe PMC)

PMID27866262 (opens in a new tab)PMCIDPMC5315729 (opens in a new tab)DOI10.1007/s00221-016-4836-9 (opens in a new tab)PepBankPUB-27866262
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Summary

The formation of oligomers and aggregates of overexpressed or mutant α-synuclein play a role in the degeneration of dopaminergic neurons in Parkinson's disease by causing dysfunction of mitochondria, reflected in their disturbed mobility and production of ROS. The mode of action and mechanisms underlying this mitochondrial impairment is still unclear. We have induced stable expression of wild-type, A30P or A53T α-synuclein in neuronally differentiated SH-SY5Y neuroblastoma cells and studied anterograde and retrograde mitochondrial trafficking in this cell model for Parkinson's disease. In contrast to wild-type and A30P, A53T α-synuclein significantly inhibited mitochondrial trafficking, at first retrogradely and in a later stage anterogradely. Accordingly, A53T α-synuclein also caused the highest increase in ROS production in the dysmobilized mitochondria in comparison to wild-type or A30P α-synuclein. Treatment with NAP, the eight amino acid peptide identified as the active component of activity-dependent neuroprotective protein (ADNP), completely annihilated the adverse effects of A53T on mitochondrial dynamics. Our results reveal that A53T α-synuclein (oligomers or aggregates) leads to the inhibition of mitochondrial trafficking, which can be rescued by NAP, suggesting the involvement of microtubule disruption in the pathophysiology of Parkinson's disease.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In SH-SY5Y cells expressing A53T alpha-synuclein, NAP completely reversed the adverse effects on mitochondrial dynamics.

    In plain wordsIn cells expressing A53T alpha-synuclein, NAP completely reversed adverse effects on mitochondrial dynamics.

    Peptide
    Davunetide
    Outcome
    Direction not reportedMitochondrial dynamics
    Study

    n: not reported in source

    Neuronally differentiated SH-SY5Y cells expressing A53T alpha-synuclein
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with NAP, the eight amino acid peptide identified as the active component of activity-dependent neuroprotective protein (ADNP), completely annihilated the adverse effects of A53T on mitochondrial dynamics.
    1 context sentence
    Summary · context
    We have induced stable expression of wild-type, A30P or A53T α-synuclein in neuronally differentiated SH-SY5Y neuroblastoma cells and studied anterograde and retrograde mitochondrial trafficking in this cell model for Parkinson's disease.

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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

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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