Evidence map›Paper›PMID 37388498›Full record

ArticleIBRO neuroscience reports2023

Component-specific reduction in perineuronal nets in senescence-accelerated mouse strains.

Hiroshi Ueno, Yu Takahashi, Shinji Murakami, Kenta Wani, Tetsuji Miyazaki, Yosuke Matsumoto, Motoi Okamoto, Takeshi Ishihara

Abstract read
In one paragraph

Article in IBRO neuroscience reports, 2023. 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

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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.

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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

8 authors.

Hiroshi UenoDepartment of Medical Technology, Kawasaki University of Medical Welfare, Okayama 701-0193, Japan.
Yu TakahashiDepartment of Psychiatry, Kawasaki Medical School, Kurashiki, 701-0192, Japan.
Shinji MurakamiDepartment of Psychiatry, Kawasaki Medical School, Kurashiki, 701-0192, Japan.
Kenta WaniDepartment of Psychiatry, Kawasaki Medical School, Kurashiki, 701-0192, Japan.
Tetsuji MiyazakiDepartment of Psychiatry, Kawasaki Medical School, Kurashiki, 701-0192, Japan.
Yosuke MatsumotoDepartment of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan.
Motoi OkamotoDepartment of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, Japan.
Takeshi IshiharaDepartment of Psychiatry, Kawasaki Medical School, Kurashiki, 701-0192, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With increased life expectancy, age-related diseases are a significant health concern in Western societies. Animal models (e.g., rodents) have been used to understand age-related changes in brain function-particularly through the senescence-accelerated mouse (SAM) strain. Previous reports have shown that the senescence-accelerated mouse propensity (SAMP)8 and SAMP10 strains have learning disabilities. In this study, we analyzed the prefrontal cortex, which is involved in cognitive function. We aimed to clarify the changes in parvalbumin-positive interneurons (PV-positive neurons), which are related to cognitive function, and perineuronal nets (PNNs), which are special extracellular matrix molecules formed around them. We performed histological analysis of PV-positive neurons and PNNs in the prefrontal cortex to elucidate the mechanism of behavioral abnormalities in SAMP8 and SAMP10 strains. Expression of Cat-315-positive PNN was not confirmed in the prefrontal cortex of SAMP10 mice. However, the density of AB1031-positive PNN, tenascin-R-positive PNN, and brevican-positive PNN decreased in the prefrontal cortex of SAMP8 and SAMP10 mice compared to that of the senescence-accelerated mouse resistance (SAMR1) mice. In addition, the density of PV-positive neurons was lower in SAMP8 mice than in SAMR1 mice. These mice, which exhibited behavioral and neuropathological phenotypes with age, showed different PV-positive neurons and PNNs in the prefrontal cortex compared with the SAMR1 mice. We believe that the results of this study will be useful for elucidating the mechanisms of age-related decline in cognitive and learning functions using SAM.

Indexed as

AgingParvalbuminPrefrontal cortexSomatosensory cortex

Identifiers

PMID37388498
PMCPMC10300471

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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.