Evidence map›Paper›PMID 19284479›Full record

ArticleNeuropathology and applied neurobiology2009

Expression of reticulon 3 in Alzheimer's disease brain.

H Kume, Y Konishi, K S Murayama, F Kametani, W Araki

Open access · greenAbstract read
In one paragraph

Article in Neuropathology and applied neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Proteolytic control of neurite outgrowth inhibitor NOGO-A by the cAMP/PKA pathway.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  7. Impact of RTN3 deficiency on expression of BACE1 and amyloid deposition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  8. Review
  9. Article
  10. Article
  11. Widespread distribution of reticulon-3 in various neurodegenerative diseases.Neuropathology : official journal of the Japanese Society of Neuropathology · 2010
    Article
  12. RTN/Nogo in forming Alzheimer's neuritic plaques.Neuroscience and biobehavioral reviews · 2010
    Article
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

5 authors at 2 institutions in 2 countries.

H KumeDepartment of Demyelinating Disease and Ageing, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Y Konishi
K S Murayama
F Kametani
W Araki
National Neuroscience Institute · SGTokyo Institute of Psychiatry · JP

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI GONZALEZ HERNANDEZ, GRACIELA · 2001 to 2020
$32.5M
NIA NIH HHS P30 AG019610NIA NIH HHS P30 AG19610
6 · The paper itself

Abstract

aimsReticulon 3 (RTN3), a member of the reticulon family of proteins, interacts with the beta-secretase, beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1), and inhibits its activity to produce beta-amyloid protein. The aim of the present study was to clarify the biological role of RTN3 in the brain and its potential involvement in the neuropathology of Alzheimer's disease (AD).

methodsWe performed immunohistochemical and biochemical analyses using a specific antibody against RTN3 to investigate the expression and subcellular localization of RTN3 in control and AD brain tissue samples.

resultsWestern blot analysis revealed no significant differences in the RTN3 levels between control and AD brains. Immunohistochemical staining showed that RTN3 immunoreactivity was predominantly localized in pyramidal neurones of the cerebral cortex. The patterns of RTN3 immunostaining were similar in control and AD cerebral cortices, and senile plaques were generally negative for RTN3. Biochemical subcellular fractionation disclosed that RTN3 colocalized with BACE1 in various fractions, including the endoplasmic reticulum and the Golgi apparatus. Double-immunofluorescence staining additionally indicated that RTN3 was localized in both endoplasmic reticulum and Golgi compartments in neurones.

conclusionsThese results show that RTN3 is primarily expressed in pyramidal neurones of the human cerebral cortex and that no clear difference of RTN3 immunoreactivity is observable between control and AD brains. Our data also suggest that there is considerable colocalization of RTN3 with BACE1 at a subcellular level.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesBlotting, WesternBrainCarrier ProteinsEndoplasmic ReticulumFemaleGolgi ApparatusHumansImmunohistochemistryMaleMembrane ProteinsAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, mouseCarrier ProteinsMembrane ProteinsNerve Tissue ProteinsRTN3 protein, humanRtn3 protein, mouse

Identifiers

PMID19284479
PMCPMC2930375
OpenAlexW2107227189

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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.