Evidence map›Paper›PMID 15051870›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Brain-specific deletion of neuropathy target esterase/swisscheese results in neurodegeneration.

Katerina Akassoglou, Brian Malester, Jixiang Xu, Lino Tessarollo, Jack Rosenbluth, Moses V Chao

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
13.6field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Pooled it
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  13. PNPLA6-Related Disorder with Levodopa-Responsive Parkinsonism.Movement disorders clinical practice · 2023
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  16. Current Knowledge on Mammalian Phospholipase AMolecules (Basel, Switzerland) · 2022
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  17. Review
  18. Insects · 2021
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17 more citing papers are in PubMed but not listed here.

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.

Katerina AkassoglouMolecular Neurobiology Program, Skirball Institute of Biomolecular Medicine, Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA.
Brian Malester
Jixiang Xu
Lino Tessarollo
Jack Rosenbluth
Moses V Chao
New York University · USCancer Genetics (United States) · USNational Cancer Institute · US

Funding

Role of Neurotrophins in the Development of the Mammalian Nervous SystemZIABC010390 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TESSAROLLO, LINO · 2009 to 2025
$14.2M
Pathology of dysmyelination and demyelinationR01NS037475 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ROSENBLUTH, JACK · 1998 to 2013
$3.3M
Role of Neurotrophins in the Development of the Mammalian Nervous SystemZ01BC010390 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TESSAROLLO, LINO · 2000 to 2008
$1.7M
MECHANISMS OF OLIGODENDROCYTE DIFFERENTIATIONR01MH059904 · NIMH · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CHAO, MOSES VICTOR · 2001 to 2004
$1.3M
NIMH NIH HHS MH59904NIMH NIH HHS R01 MH059904NINDS NIH HHS NS37475NINDS NIH HHS R01 NS037475
6 · The paper itself

Abstract

Neuropathy target esterase (NTE) is a neuronal membrane protein originally identified for its property to be modified by organo-phosphates (OPs), which in humans cause neuropathy characterized by axonal degeneration. Drosophila mutants for the homolog gene of NTE, swisscheese (sws), indicated a possible involvement of sws in the regulation of axon-glial cell interaction during glial wrapping. However, the role of NTE/sws in mammalian brain pathophysiology remains unknown. To investigate NTE function in vivo, we used the cre/loxP site-specific recombination strategy to generate mice with a specific deletion of NTE in neuronal tissues. Here we show that loss of NTE leads to prominent neuronal pathology in the hippocampus and thalamus and also defects in the cerebellum. Absence of NTE resulted in disruption of the endoplasmic reticulum, vacuolation of nerve cell bodies, and abnormal reticular aggregates. Thus, these results identify a physiological role for NTE in the nervous system and indicate that a loss-of-function mechanism may contribute to neurodegenerative diseases characterized by vacuolation and neuronal loss.

Indexed as

AnimalsBrainCarboxylic Ester HydrolasesCells, CulturedEndoplasmic ReticulumImmunohistochemistryMiceMicroscopy, ElectronRatsCarboxylic Ester Hydrolasesneurotoxic esterase

Identifiers

PMID15051870
PMCPMC387376
OpenAlexW1998799810

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.