Evidence map›Paper›PMID 28438696›Full record

ArticleMolecular and cellular neurosciences2017

Altered temporal lobe white matter lipid ion profiles in an experimental model of sporadic Alzheimer's disease.

Ming Tong, Raiane Leão, Gina V Vimbela, Emine B Yalcin, Jared Kay, Alexander Krotow, Suzanne M de la Monte

Abstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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  8. Rapid Peak Alignment for MALDI-TOF Lipid Analysis.Journal of bioanalytical methods and techniques · 2021
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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 5 institutions in 2 countries.

Ming TongLiver Research Center, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Division of Gastroenterology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Department of Medicine, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States.
Raiane LeãoFederal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Gina V VimbelaDepartment of Chemical Engineering, California State University, Long Beach, CA, United States.
Emine B YalcinLiver Research Center, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States.
Jared KayLiver Research Center, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States.
Alexander KrotowPathobiology Graduate Program, Brown University, United States.
Suzanne M de la MonteLiver Research Center, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Division of Gastroenterology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Division of Neuropathology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Department of Medicine, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Department of Pathology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Department of Neurology, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States; Department of Neurosurgery, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, RI, United States. Electronic address: Suzanne_DeLaMonte_MD@Brown.edu.
Brown University · USCalifornia State University, Long Beach · USJohn Brown University · USRhode Island Hospital · USUniversidade Federal de Minas Gerais · BR

Funding

FASD Inhibition of ASPH-Notch Mediates Adolescent Cerebral White Matter Pathology-Potential Utility of Non-invasive Extracellular Vesicle AssaysR01AA011431 · NIAAA · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI SUZANNE M. DE LA MONTE · 1996 to 2026
$5.4M
Ethanol, IRS-1 Signaling and Neuronal MigrationR37AA011431 · NIAAA · RHODE ISLAND HOSPITAL · PI DE LA MONTE, SUZANNE M. · 2009 to 2018
$3.7M
Clinical Evaluation of T3D-959 as a Potential Disease Remedial Therapeutic for the Treatment of Alzheimer's DiseaseR44AG049510 · NIA · T3D THERAPEUTICS, INC. · PI DE LA MONTE, SUZANNE M., DIDSBURY, JOHN · 2015 to 2016
$1.9M
Short-Term Training Program to Increase Diversity in Health-Related ResearchR25HL088992 · NHLBI · BROWN UNIVERSITY · PI ABID, RUHUL, DIAZ, JOSEPH A · 2007 to 2024
$1.9M
ETHANOL, INSULIN/IGF SIGNALING AND NEURONAL MIGRATIONR56AA011431 · NIAAA · RHODE ISLAND HOSPITAL · PI DE LA MONTE, SUZANNE M. · 2008 to 2008
$312k
NHLBI NIH HHS R25 HL088992NIAAA NIH HHS R01 AA011431NIAAA NIH HHS R37 AA011431NIAAA NIH HHS R56 AA011431NIA NIH HHS R44 AG049510
6 · The paper itself

Abstract

backgroundWhite matter is an early and important yet under-evaluated target of Alzheimer's disease (AD). Metabolic impairments due to insulin and insulin-like growth factor resistance contribute to white matter degeneration because corresponding signal transduction pathways maintain oligodendrocyte function and survival.

methodsThis study utilized a model of sporadic AD in which adult Long Evans rats administered intracerebral streptozotocin (i.c. STZ) developed AD-type neurodegeneration. Temporal lobe white matter lipid ion profiles were characterized by matrix-assisted laser desorption/ionization-imaging mass spectrometry (MALDI-IMS).

resultsAlthough the lipid ion species expressed in the i.c. STZ and control groups were virtually identical, i.c. STZ mainly altered the abundances of various lipid ions. Correspondingly, the i.c. STZ group was distinguished from control by principal component analysis and data bar plots. i.c. STZ mainly reduced expression of lipid ions with low m/z's (less than 810) as well as the upper range m/z lipids (m/z 964-986), and increased expression of lipid ions with m/z's between 888 and 937. Phospholipids were mainly included among the clusters inhibited by i.c. STZ, while both sulfatides and phospholipids were increased by i.c. STZ. However, Chi-Square analysis demonstrated significant i.c. STZ-induced trend reductions in phospholipids and increases in sulfatides (P<0.00001).

conclusionsThe i.c. STZ model of sporadic AD is associated with broad and sustained abnormalities in temporal lobe white matter lipids. The findings suggest that the i.c. STZ model could be used for pre-clinical studies to assess therapeutic measures for their ability to restore white matter integrity in AD.

Indexed as

Alzheimer DiseaseAnimalsDisease Models, AnimalInsulinIonsLipid MetabolismLipidsMaleRats, Long-EvansStreptozocinTemporal LobeWhite MatterInsulinIonsLipidsStreptozocinAlzheimerImaging mass spectrometryMALDIStreptozotocinWhite matter degeneration

Identifiers

PMID28438696
PMCPMC5507369
OpenAlexW2606626052

What OpenQuestion holds

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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.