Evidence map›Paper›PMID 37699718›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2023

Genetic Reduction of Insulin Signaling Mitigates Amyloid-β Deposition by Promoting Expression of Extracellular Matrix Proteins in the Brain.

Toshiharu Sano, Toshitaka Ochiai, Takeru Nagayama, Ayaka Nakamura, Naoto Kubota, Takashi Kadowaki, Tomoko Wakabayashi, Takeshi Iwatsubo

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Changes in the Extracellular Matrix with Aging: A Larger Role in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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

8 authors at 1 institution in 1 country.

Toshiharu SanoDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Toshitaka OchiaiDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Takeru NagayamaDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Ayaka NakamuraDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Naoto KubotaDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Takashi KadowakiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Tomoko WakabayashiDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan tomoko-wakabayashi@umin.ac.jp iwatsubo@m.u-tokyo.ac.jp.
Takeshi IwatsuboDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan tomoko-wakabayashi@umin.ac.jp iwatsubo@m.u-tokyo.ac.jp.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The insulin/IGF-1 signaling (IIS) regulates a wide range of biological processes, including aging and lifespan, and has also been implicated in the pathogenesis of Alzheimer's disease (AD). We and others have reported that reduced signaling by genetic ablation of the molecules involved in IIS (e.g., insulin receptor substrate 2 [IRS-2]) markedly mitigates amyloid plaque formation in the brains of mouse models of AD, although the molecular underpinnings of the amelioration remain unsolved. Here, we revealed, by a transcriptomic analysis of the male murine cerebral cortices, that the expression of genes encoding extracellular matrix (ECM) was significantly upregulated by the loss of IRS-2. Insulin signaling activity negatively regulated the phosphorylation of Smad2 and Smad3 in the brain, and suppressed TGF-β/Smad-dependent expression of a subset of ECM genes in brain-derived cells. The ECM proteins inhibited Aβ fibril formation

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalExtracellular Matrix ProteinsInsulinInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsMaleMiceMice, TransgenicPlaque, AmyloidTransforming Growth Factor betaAmyloid beta-PeptidesAmyloid beta-Protein PrecursorExtracellular Matrix ProteinsInsulinInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsTransforming Growth Factor betaAlzheimer's diseaseamyloid βextracellular matrixinsulin signaling

Identifiers

PMID37699718
PMCPMC10601373
OpenAlexW4386647248

What OpenQuestion holds

Textmetadata
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.