Evidence map›Paper›PMID 33125735›Full record

ArticleJournal of pineal research2021

The melatonin metabolite N1-acetyl-5-methoxykynuramine facilitates long-term object memory in young and aging mice.

Hikaru Iwashita, Yukihisa Matsumoto, Yusuke Maruyama, Kazuki Watanabe, Atsuhiko Chiba, Atsuhiko Hattori

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Journal of pineal research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 38 citations in OpenAlex.

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  18. Melatonin Improves Short-Term Spatial Memory in a Mouse Model of Alzheimer's Disease.Degenerative neurological and neuromuscular disease · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Hikaru IwashitaDepartment of Biology, College of Liberal Arts and Sciences, Tokyo Medical and Dental University, Chiba, Japan.
Yukihisa MatsumotoDepartment of Biology, College of Liberal Arts and Sciences, Tokyo Medical and Dental University, Chiba, Japan.
Yusuke MaruyamaDepartment of Biology, College of Liberal Arts and Sciences, Tokyo Medical and Dental University, Chiba, Japan.
Kazuki WatanabeDepartment of Biology, College of Liberal Arts and Sciences, Tokyo Medical and Dental University, Chiba, Japan.ORCID https://orcid.org/0000-0003-1860-4358
Atsuhiko ChibaDepartment of Materials and Life Sciences, Faculty of Science and Technology, Sophia University, Tokyo, Japan.
Atsuhiko HattoriDepartment of Biology, College of Liberal Arts and Sciences, Tokyo Medical and Dental University, Chiba, Japan.ORCID https://orcid.org/0000-0002-4961-3129
Tokyo Medical and Dental University · JPSophia University · JP

Funding

Grant-in-Aid for Scientific Research at Tokyo Medical and Dental UniversityJSPS KAKENHI JP18K11016
6 · The paper itself

Abstract

Melatonin (MEL) has been reported to enhance cognitive processes, making it a potential treatment for cognitive decline. However, the role of MEL's metabolites, N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N1-acetyl-5-methoxykynuramine (AMK), in these effects are unknown. The current study directly investigated the acute effects of systemic MEL, AFMK, and AMK on novel object recognition. We also analyzed MEL, AFMK, and AMK levels in hippocampus and temporal lobe containing the perirhinal cortex following systemic MEL and AMK treatment. AMK administered post-training had a more potent effect on object memory than MEL and AFMK. AMK was also able to rescue age-associated declines in memory impairments when object memory was tested up to 4 days following training. Results from administering AMK at varying times around the training trial and the metabolism time course in brain tissue suggest that AMK's memory-enhancing effects reflect memory consolidation. Furthermore, inhibiting the MEL-to-AMK metabolic pathway disrupted object memory at 24 hours post-training, suggesting that endogenous AMK might play an important role in long-term memory formation. This is the first study to report that AMK facilitates long-term object memory performance in mice, and that MEL crosses the blood-brain barrier and is immediately converted to AMK in brain tissue. Overall, these results support AMK as a potential therapeutic agent to improve or prevent memory decline.

Indexed as

Age FactorsAnimalsBehavior, AnimalBiotransformationHippocampusKynuramineMaleMelatoninMemory, Long-TermMiceMice, Inbred ICROpen Field TestTemporal LobeTime FactorsKynuramineMelatoninN-acetyl-5-methoxy kynurenamineN-acetyl-N-formyl-5-methoxykynurenamineaginglong-term memorymelatoninN1-acetly-5-methoxykynuramineN1-acetyl-N2-formyl-5-methoxykynuraminenovel object recognitionshort-term memory

Identifiers

PMID33125735
PMCPMC7816253
OpenAlexW3095587932

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.