Evidence map›Paper›PMID 30604097›Full record

ArticleAmino acids2019

Altered brain arginine metabolism in a mouse model of tauopathy.

Pranav Vemula, Yu Jing, Hu Zhang, Jerry B Hunt, Leslie A Sandusky-Beltran, Daniel C Lee, Ping Liu

Abstract read
In one paragraph

Article in Amino acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Arginase 1 Insufficiency Precipitates Amyloid-Frontiers in immunology · 2020
    Article
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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

7 authors at 4 institutions in 2 countries.

Pranav VemulaDepartment of Anatomy, School of Biomedical Sciences, Brain Health Research Centre, University of Otago, Dunedin, New Zealand.
Yu JingDepartment of Anatomy, School of Biomedical Sciences, Brain Health Research Centre, University of Otago, Dunedin, New Zealand.
Hu ZhangSchool of Pharmacy, Brain Health Research Centre, University of Otago, Dunedin, New Zealand.
Jerry B HuntByrd Alzheimer's Institute, College of Pharmacy and Pharmaceutical Sciences, University of South Florida, Florida, USA.
Leslie A Sandusky-BeltranByrd Alzheimer's Institute, College of Pharmacy and Pharmaceutical Sciences, University of South Florida, Florida, USA.
Daniel C LeeByrd Alzheimer's Institute, College of Pharmacy and Pharmaceutical Sciences, University of South Florida, Florida, USA.
Ping LiuDepartment of Anatomy, School of Biomedical Sciences, Brain Health Research Centre, University of Otago, Dunedin, New Zealand. ping.liu@otago.ac.nz.
Brain Research New Zealand · NZUSF Health Byrd Alzheimer's Institute · USUniversity of Otago · NZUniversity of South Florida · US

Funding

Emerging Roles of Higher-order Polyamines During TauopathiesR01AG054559 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI LEE, DANIEL CARL · 2017 to 2021
$2.4M
NIA NIH HHS R01 AG054559
6 · The paper itself

Abstract

Tauopathies consist of intracellular accumulation of hyperphosphorylated and aggregated microtubule protein tau, which remains a histopathological feature of Alzheimer's disease (AD) and frontotemporal dementia. L-Arginine is a semi-essential amino acid with a number of bioactive molecules. Its downstream metabolites putrescine, spermidine, and spermine (polyamines) are critically involved in microtubule assembly and stabilization. Recent evidence implicates altered arginine metabolism in the pathogenesis of AD. Using high-performance liquid chromatographic and mass spectrometric assays, the present study systematically determined the tissue concentrations of L-arginine and its nine downstream metabolites in the frontal cortex, hippocampus, parahippocampal region, striatum, thalamus, and cerebellum in male PS19 mice-bearing human tau P301S mutation at 4, 8, and 12-14 months of age. As compared to their wild-type littermates, PS19 mice displayed early and/or prolonged increases in L-ornithine and altered polyamine levels with age. There were also genotype- and age-related changes in L-arginine, L-citrulline, glutamine, glutamate, and γ-aminobutyric acid in a region- and/or chemical-specific manner. The results demonstrate altered brain arginine metabolism in PS19 mice with the most striking changes in L-ornithine, polyamines, and glutamate, indicating a shift of L-arginine metabolism to favor the arginase-polyamine pathway. Given the role of polyamines in maintaining microtubule stability, the functional significance of these changes remains to be explored in future research.

Indexed as

Disease Models, AnimalAnimalsArginineBrainHumansMaleMiceMice, TransgenicTauopathiestau ProteinsArgininetau ProteinsArginine metabolismGlutamateHippocampusL-OrnithinePolyaminesTauopathy

Identifiers

PMID30604097
PMCPMC6431576
OpenAlexW2907627683

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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.