Evidence map›Paper›PMID 31016475›Full record

ArticleMolecular neurobiology2019

Reverting Metabolic Dysfunction in Cortex and Cerebellum of APP/PS1 Mice, a Model for Alzheimer's Disease by Pioglitazone, a Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) Agonist.

Kai Lun Chang, Ling Rong Wong, Hai Ning Pee, Shili Yang, Paul Chi-Lui Ho

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  5. Mitochondria in health, disease, and aging.Physiological reviews · 2023
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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

5 authors at 1 institution in 2 countries.

Kai Lun ChangDepartment of Pharmacy, Faculty of Science, National University of Singapore, Singapore, Republic of Singapore.
Ling Rong WongDepartment of Pharmacy, Faculty of Science, National University of Singapore, Singapore, Republic of Singapore.
Hai Ning PeeDepartment of Pharmacy, Faculty of Science, National University of Singapore, Singapore, Republic of Singapore.
Shili YangDepartment of Pharmacy, Faculty of Science, National University of Singapore, Singapore, Republic of Singapore. lsiysh@nus.edu.sg.
Paul Chi-Lui HoDepartment of Pharmacy, Faculty of Science, National University of Singapore, Singapore, Republic of Singapore. phahocl@nus.edu.sg.ORCID http://orcid.org/0000-0001-9213-7116
National University of Singapore · SG

Funding

National University of Singapore R148-000-180-112
6 · The paper itself

Abstract

Identification of molecular mechanisms underlying early-stage Alzheimer's disease (AD) is important for the development of new therapies against and diagnosis of AD. In this study, gas chromatography time-of-flight mass spectrometry (GC-TOF-MS)-based metabolomics approach was employed to investigate the metabolic profiles in plasma and brain tissues harvested from 5-month-old APP/PS1 transgenic mice and their wildtype counterparts. Since different brain regions were expected to have their own distinct metabolic signals, four different brain regions, namely cortex, hippocampus, midbrain and cerebellum tissues, were dissected and had their metabolic profiles studied separately. Biochemical assays were also performed on plasma and brain cortex tissue of transgenic mice and wildtype mice, with a focus on mitochondrial health. Amyloid precursor protein and amyloid-β levels in plasma, brain cortex tissue and mitochondria fractions isolated from brain cortex were measured to assess the amyloid pathology. Our findings include the observation of extensive metabolic alterations in cortex and cerebellum of APP/PS1 mice, but not in their hippocampus, midbrain and plasma. The major pathways affected in cortex and cerebellum of APP/PS1 mice were closely related to impaired energy metabolism and perturbation of amino acid metabolism in these mice. APP/PS1 mice also exhibited higher amyloid-β40 and amyloid-β42 in their cortex, accumulation of mitochondria APP in their cortex, and presented an altered oxidative state in their brain. Treatment with the peroxisome proliferator-activated receptor gamma (PPARγ) agonist pioglitazone (PIO) successfully restored the energy metabolism, lowered amyloid-β levels and afforded the APP/PS1 mice a better antioxidative capacity in their cortex.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCatalaseCerebellumCerebral CortexCitrate (si)-SynthaseDiscriminant AnalysisDisease Models, AnimalFemaleHippocampusL-Lactate DehydrogenaseMaleMetabolomicsMice, TransgenicMitochondriaAmyloid beta-Protein PrecursorCatalaseCitrate (si)-SynthaseL-Lactate DehydrogenasePioglitazonePPAR gammaPresenilin-1Superoxide DismutaseAlzheimer’s diseaseAPP/PS1 miceMetabolic profilingMitochondriaPioglitazone

Identifiers

PMID31016475
OpenAlexW2941272239

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.