Evidence map›Paper›PMID 23882219›Full record

ArticleFrontiers in physiology2013

Using neurolipidomics to identify phospholipid mediators of synaptic (dys)function in Alzheimer's Disease.

Steffany A L Bennett, Nicolas Valenzuela, Hongbin Xu, Bettina Franko, Stephen Fai, Daniel Figeys

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

48 citing papers in PubMed, 83 citations in OpenAlex.

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  12. Machine Learning and Hybrid Methods for Metabolic Pathway Modeling.Methods in molecular biology (Clifton, N.J.) · 2023
    Review
  13. Lipids and Secretory Vesicle Exocytosis.Advances in neurobiology · 2023
    Article
  14. Lipid Profiling in Alzheimer's Disease.Advances in experimental medicine and biology · 2023
    Article
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  17. Review
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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

6 authors at 3 institutions in 1 country.

Steffany A L BennettOttawa Institute of Systems Biology Ottawa, ON, Canada ; Neural Regeneration Laboratory, Department of Biochemistry, Microbiology, and Immunology, University of Ottawa Ottawa, ON, Canada ; CIHR Training Program in Neurodegenerative Lipidomics, Department of Biochemistry, Microbiology, and Immunology, University of Ottawa Ottawa, ON, Canada.
Nicolas Valenzuela
Hongbin Xu
Bettina Franko
Stephen Fai
Daniel Figeys
Ottawa Institute of Systems BiologyCarleton University · CAUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Not all of the mysteries of life lie in our genetic code. Some can be found buried in our membranes. These shells of fat, sculpted in the central nervous system into the cellular (and subcellular) boundaries of neurons and glia, are themselves complex systems of information. The diversity of neural phospholipids, coupled with their chameleon-like capacity to transmute into bioactive molecules, provides a vast repertoire of immediate response second messengers. The effects of compositional changes on synaptic function have only begun to be appreciated. Here, we mined 29 neurolipidomic datasets for changes in neuronal membrane phospholipid metabolism in Alzheimer's Disease (AD). Three overarching metabolic disturbances were detected. We found that an increase in the hydrolysis of platelet activating factor precursors and ethanolamine-containing plasmalogens, coupled with a failure to regenerate relatively rare alkyl-acyl and alkenyl-acyl structural phospholipids, correlated with disease severity. Accumulation of specific bioactive metabolites [i.e., PC(O-16:0/2:0) and PE(P-16:0/0:0)] was associated with aggravating tau pathology, enhancing vesicular release, and signaling neuronal loss. Finally, depletion of PI(16:0/20:4), PI(16:0/22:6), and PI(18:0/22:6) was implicated in accelerating Aβ42 biogenesis. Our analysis further suggested that converging disruptions in platelet activating factor, plasmalogen, phosphoinositol, phosphoethanolamine (PE), and docosahexaenoic acid metabolism may contribute mechanistically to catastrophic vesicular depletion, impaired receptor trafficking, and morphological dendritic deformation. Together, this analysis supports an emerging hypothesis that aberrant phospholipid metabolism may be one of multiple critical determinants required for Alzheimer disease conversion.

Indexed as

Alzheimer's Diseaseamyloid-betalipidomicsmass spectrometryneurolipidomicsphospholipidsuper resolution nanoscopysynaptotoxicity

Identifiers

PMID23882219
PMCPMC3712192
OpenAlexW2065461128

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.