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Study · In vitro (cells) · 2021

3 results

Nmnat2 attenuates amyloidogenesis and up-regulates ADAM10 in AMPK activity-dependent manner.

Cheng XS, Shi FX, Zhao KP, Lin W, Li XY, Zhang J, Bu YY, Zhu R, Li XH, Duan DX, Ji XY, Wei JS, Wang JZ, Du J, Zhou XW

Aging13 Oct 2021Cited by 17 (Europe PMC)

PMID34644262 (opens in a new tab)PMCIDPMC8580354 (opens in a new tab)DOI10.18632/aging.203634 (opens in a new tab)PepBankPUB-34644262
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Summary

Amyloid-β (Aβ) accumulating is considered as a causative factor for formation of senile plaque in Alzheimer's disease (AD), but its mechanism is still elusive. The Nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2), a key redox cofactor for energy metabolism, is reduced in AD. Accumulative evidence has shown that the decrease of α-secretase activity, a disintegrin and metalloprotease domain 10 (ADAM10), is responsible for the increase of Aβ productions in AD patient's brain. Here, we observe that the activity of α-secretase ADAM10 and levels of Nmnat2 are significantly decreased, meanwhile there is a simultaneous elevation of Aβ in Tg2576 mice. Over-expression of Nmnat2 increases the mRNA expression of α-secretase ADAM10 and its activity and inhibits Aβ production in N2a/APPswe cells, which can be abolished by Compound C, an AMPK antagonist, suggesting that AMPK is involved in over-expression of Nmnat2 against Aβ production. The further assays demonstrate that Nmnat2 activates AMPK by up-regulating the ratio of NAD+/NADH, moreover AMPK agonist AICAR can also increase ADAM10 activity and reduces Aβ1-40/1-42. Taken together, Nmnat2 suppresses Aβ production and up-regulates ADAM10 in AMPK activity-dependent manner, suggesting that Nmnat2 may serve as a new potential target in arresting AD.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01LabIn vitro (cells)Mechanism

    In cellular assays, AICAR increased ADAM10 activity.

    In plain wordsIn cells, AICAR increased ADAM10 activity.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseADAM10 activity
    Study

    n: not reported in source

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

    Source sentences

    Summary
    moreover AMPK agonist AICAR can also increase ADAM10 activity and reduces Aβ1-40/1-42.
  2. 02LabIn vitro (cells)Mechanism

    In cellular assays, AICAR reduced Aβ1-40.

    In plain wordsIn cells, AICAR reduced Aβ1-40.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAβ1-40
    Study

    n: not reported in source

    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    moreover AMPK agonist AICAR can also increase ADAM10 activity and reduces Aβ1-40/1-42.
  3. 03LabIn vitro (cells)Mechanism

    In cellular assays, AICAR reduced Aβ1-42.

    In plain wordsIn cells, AICAR reduced Aβ1-42.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAβ1-42
    Study

    n: not reported in source

    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    moreover AMPK agonist AICAR can also increase ADAM10 activity and reduces Aβ1-40/1-42.

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 3Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 2

    21 Oct 2026, 12:50 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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