Evidence map›Paper›PMID 39122814›Full record

ArticleScientific reports2024

Suppression of the amyloidogenic metabolism of APP and the accumulation of Aβ by alcadein α in the brain during aging.

Keiko Honda, Hiroo Takahashi, Saori Hata, Ruriko Abe, Takashi Saito, Takaomi C Saido, Hidenori Taru, Yuriko Sobu, Kanae Ando, Tohru Yamamoto and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

11 authors.

Keiko Honda *Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Hiroo Takahashi *Department of Molecular Neurobiology, Faculty of Medicine, Kagawa University, Miki-cho, 761-0793, Japan.
Saori Hata *Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Ruriko AbeAdvanced Prevention and Research Laboratory for Dementia, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Takashi SaitoDepartment of Neurocognitive Science, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, 467-8601, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science Institute, Wako, 351-0198, Japan.
Hidenori TaruLaboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Yuriko SobuLaboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan.
Kanae AndoDepartment of Biological Sciences, Graduate School of Science, Tokyo Metropolitan University, Hachioji, Tokyo, 192-0397, Japan.
Tohru YamamotoDepartment of Molecular Neurobiology, Faculty of Medicine, Kagawa University, Miki-cho, 761-0793, Japan. yamamoto.toru@kagawa-u.ac.jp.
Toshiharu SuzukiLaboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, 060-0812, Japan. suzuki_t@tmu.ac.jp.

Funding

Japan Agency for Medical Research and Development JP23dk0207059Japan Society for the Promotion of Science JP22K06597Japan Society for the Promotion of Science JP22K15270Japan Society for the Promotion of Science JP23K06840
6 · The paper itself

Abstract

Generation and accumulation of amyloid-β (Aβ) protein in the brain are the primary causes of Alzheimer's disease (AD). Alcadeins (Alcs composed of Alcα, Alcβ and Alcγ family) are a neuronal membrane protein that is subject to proteolytic processing, as is Aβ protein precursor (APP), by APP secretases. Previous observations suggest that Alcs are involved in the pathophysiology of Alzheimer's disease (AD). Here, we generated new mouse App

Indexed as

AgingAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesBrainAlzheimer DiseaseAnimalsAspartic Acid EndopeptidasesCalcium-Binding ProteinsMiceMice, KnockoutNerve Tissue ProteinsNeuronsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, mouseCalcium-Binding ProteinsNerve Tissue Proteins

Identifiers

PMID39122814
PMCPMC11316129

What OpenQuestion holds

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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.