Evidence map›Paper›PMID 35203488›Full record

ArticleBiomedicines2022

Relationship between Cognitive Dysfunction and Age-Related Variability in Oxidative Markers in Isolated Mitochondria of Alzheimer's Disease Transgenic Mouse Brains.

Naoki Yoshida, Yugo Kato, Hirokatsu Takatsu, Koji Fukui

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

Article in Biomedicines, 2022. 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
2.9field-weighted citation impact, top 8% 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, 25 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Naoki YoshidaMolecular Cell Biology Laboratory, Department of Systems Engineering and Science, Graduate School of Engineering and Science, Shibaura Institute of Technology, Fukasaku 307, Minuma-ku, Saitama 337-8570, Japan.
Yugo KatoMolecular Cell Biology Laboratory, Department of Functional Control Systems, Graduate School of Engineering and Science, Shibaura Institute of Technology, Fukasaku 307, Minuma-ku, Saitama 337-8570, Japan.ORCID 0000-0002-8357-0986
Hirokatsu TakatsuDepartment of Medical Technology, Faculty of Health Sciences, Kyorin University, Shimorenjaku 5-4-1, Mitaka, Tokyo 181-8612, Japan.ORCID 0000-0001-5666-3231
Koji FukuiMolecular Cell Biology Laboratory, Department of Systems Engineering and Science, Graduate School of Engineering and Science, Shibaura Institute of Technology, Fukasaku 307, Minuma-ku, Saitama 337-8570, Japan.ORCID 0000-0003-2748-3228
Shibaura Institute of Technology · JPKyorin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many neurodegenerative disorders, including Alzheimer's disease (AD), are strongly associated with the accumulation of oxidative damage. Transgenic animal models are commonly used to elucidate the pathogenic mechanism of AD. Beta amyloid (Aβ) and tau hyperphosphorylation are very famous hallmarks of AD and well-studied, but the relationship between mitochondrial dysfunction and the onset and progression of AD requires further elucidation. In this study we used transgenic mice (the strain name is 5xFAD) at three different ages (3, 6, and 20 months old) as an AD model. Cognitive impairment in AD mice occurred in an age-dependent manner. Aβ1-40 expression significantly increased in an age-dependent manner in all brain regions with or without AD, and Aβ1-42 expression in the hippocampus increased at a young age. In a Western blot analysis using isolated mitochondria from three brain regions (cerebral cortex, cerebellum, and hippocampus), NMNAT-3 expression in the hippocampi of aged AD mice was significantly lower than that of young AD mice. SOD-2 expression in the hippocampi of AD mice was lower than for the age-matched controls. However, 3-NT expression in the hippocampi of AD mice was higher than for the age-matched controls. NQO-1 expression in the cerebral cortex of AD mice was higher than for the age-matched controls at every age that we examined. However, hippocampal NQO-1 expression in 6-month-old AD mice was significantly lower than in 3-month-old AD mice. These results indicate that oxidative stress in the hippocampi of AD mice is high compared to other brain regions and may induce mitochondrial dysfunction via oxidative damage. Protection of mitochondria from oxidative damage may be important to maintain cognitive function.

Indexed as

Alzheimer’s diseasecognitive impairmentmitochondriaoxidative stressreactive oxygen species

Identifiers

PMID35203488
PMCPMC8869326
OpenAlexW4210556119

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.