Evidence map›Paper›PMID 27956354›Full record

ArticleBiochimica et biophysica acta. Proteins and proteomics2017

MALDI imaging delineates hippocampal glycosphingolipid changes associated with neurotoxin induced proteopathy following neonatal BMAA exposure.

Oskar Karlsson, Wojciech Michno, Yusuf Ransome, Jörg Hanrieder

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

Article in Biochimica et biophysica acta. Proteins and proteomics, 2017. 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
0.7field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 13 citations in OpenAlex.

  1. 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

4 authors at 4 institutions in 3 countries.

Oskar KarlssonCenter for Molecular Medicine, Department of Clinical Neuroscience, Karolinska Institute, 171 76 Stockholm, Sweden; Department of Pharmaceutical Biosciences, Toxicology and Drug Safety, Uppsala University, Box 591, 751 24 Uppsala, Sweden; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Wojciech MichnoDepartment of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal Hospital, House V, 431 80 Mölndal, Sweden.
Yusuf RansomeDepartment of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA.
Jörg HanriederDepartment of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Mölndal Hospital, House V, 431 80 Mölndal, Sweden; Department of Chemistry and Chemical Engineering, Analytical Chemistry, Chalmers University of Technology, Kemivägen 10, 412 96 Gothenburg, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, University College London, Queen Square, WC1N 3BG London, UK. Electronic address: jh@gu.se.
Harvard University · USNational Hospital for Neurology and Neurosurgery · GBUniversity of Gothenburg · SEUppsala University · SE

Funding

The Brown Initiative in HIV and AIDS Clinical Research for Minority CommunitiesR25MH083620 · NIMH · MIRIAM HOSPITAL · PI NUNN, AMY STEWART · 2008 to 2025
$3.7M
NIMH NIH HHS R25 MH083620
6 · The paper itself

Abstract

The environmental toxin β-N-methylamino-L-alanine (BMAA) has been proposed to contribute to neurodegenerative diseases. We have previously shown that neonatal exposure to BMAA results in dose-dependent cognitive impairments, proteomic alterations and progressive neurodegeneration in the hippocampus of adult rats. A high BMAA dose (460mg/kg) also induced intracellular fibril formation, increased protein ubiquitination and enrichment of proteins important for lipid transport and metabolism. The aim of this study was therefore to elucidate the role of neuronal lipids in BMAA-induced neurodegeneration. By using matrix assisted laser desorption/ionization imaging mass spectrometry (MALDI IMS), we characterized the spatial lipid profile in the hippocampus of six month-old rats that were treated neonatally (postnatal days 9-10) with 460mg/kg BMAA. Multivariate statistical analysis revealed long-term changes in distinct ganglioside species (GM, GD, GT) in the dentate gyrus. These changes could be a consequence of direct effects on ganglioside biosynthesis through the b-series (GM3-GD3-GD2-GD1b-GT1b) and may be linked to astrogliosis. Complementary immunohistochemistry experiments towards GFAP and S100β further verified the role of increased astrocyte activity in BMAA-induced brain damage. This highlights the potential of imaging MS for probing chemical changes associated with neuropathological mechanisms in situ. This article is part of a Special Issue entitled: MALDI Imaging, edited by Dr. Corinna Henkel and Prof. Peter Hoffmann.

Indexed as

Amino Acids, DiaminoAnimalsAnimals, NewbornAstrocytesCyanobacteria ToxinsDentate GyrusFemaleGangliosidesGliosisGlycosphingolipidsHippocampusLipid MetabolismLipidsNeurodegenerative DiseasesNeurotoxinsPregnancyAmino Acids, Diaminobeta-N-methylamino-L-alanineCyanobacteria ToxinsGangliosidesGlycosphingolipidsLipidsNeurotoxinsBeta-N-methylamino-L-alanine (BMAA)Environmental toxinGliosisGlycosphingolipidsImaging mass spectrometryProtein pathology

Identifiers

PMID27956354
PMCPMC6010999
OpenAlexW2560423033

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.