Evidence map›Paper›PMID 40138382›Full record

ArticlePloS one2025

Naturido alleviates amyloid β1-42-induced adverse effects in a transgenic Caenorhabditis elegans model of Alzheimer's disease.

Piyamas Sillapakong, Tokumitsu Wakabayashi, Koichi Suzuki

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Frontiers in aging neuroscience · 2026
    Review
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

3 authors.

Piyamas SillapakongBiococoon Laboratories, Inc., Morioka, Iwate, Japan.
Tokumitsu WakabayashiDepartment of Chemistry and Biological Sciences, Faculty of Science and Engineering, Iwate University, Morioka, Iwate, Japan.ORCID 0000-0003-4037-6427
Koichi SuzukiBiococoon Laboratories, Inc., Morioka, Iwate, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder primarily associated with aging. While the amyloid hypothesis is not the only explanation for AD pathogenesis, it is widely recognized that the accumulation of amyloid β (Aβ) protein triggers pathological changes in the brains of patients. In a previous study, we showed that Naturido, a cyclic peptide derived from the medicinal fungus (Isaria japonica) grown on domestic silkworms (Bombyx mori), could reverse several age-related deficits in senescence-accelerated mice. In this study, we explored the potential of Naturido to reduce Aβ-related toxicity in transgenic Caenorhabditis elegans models of AD, where human Aβ1-42 protein is overexpressed in neurons. Our results demonstrated that Naturido administration alleviated various phenotypes, including Aβ-induced impairment in associative learning, serotonin hypersensitivity, and locomotion in the transgenic C. elegans. These findings suggest the potential of Naturido as a candidate molecule for the prevention and/or treatment of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCaenorhabditis elegansPeptide FragmentsAnimalsAnimals, Genetically ModifiedDisease Models, AnimalHumansLocomotionAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide Fragments

Identifiers

PMID40138382
PMCPMC11940425

What Socratic holds

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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 Socratic graph.