Evidence map›Paper›PMID 23313024›Full record

ArticleThe American journal of pathology2013

Axonopathy in an α-synuclein transgenic model of Lewy body disease is associated with extensive accumulation of C-terminal-truncated α-synuclein.

Dora Games, Peter Seubert, Edward Rockenstein, Christina Patrick, Margarita Trejo, Kiren Ubhi, Benjamin Ettle, Majid Ghassemiam, Robin Barbour, Dale Schenk and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
6.3field-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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Recombinant Antibody Fragments for Immunotherapy of Parkinson's Disease.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024
    Review
  12. Liquid-liquid phase separation and conformational strains ofFrontiers in molecular neuroscience · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  19. Article
  20. Article

8 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

12 authors at 3 institutions in 2 countries.

Dora GamesNeotope Biosciences, South San Francisco, California, USA.
Peter Seubert
Edward Rockenstein
Christina Patrick
Margarita Trejo
Kiren Ubhi
Benjamin Ettle
Majid Ghassemiam
Robin Barbour
Dale Schenk
Silke Nuber
Eliezer Masliah
University of California, San Diego · USUniversity of California, San Francisco · USUniversitätsklinikum Erlangen · DE

Funding

VIRUS-INDUCED BRAIN PATHOLOGYP50AG005131 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALASKO, DOUGLAS R · 1985 to 2018
$55.4M
Tissue Culture CoreP01AG022074 · NIA · J. DAVID GLADSTONE INSTITUTES · PI MASLIAH, ELIEZER · 2003 to 2012
$27.0M
Viral VectorsP01AG010435 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TUSZYNSKI, MARK H. · 1991 to 2014
$20.9M
Studies on Diagnosis, Pathophysiology, and Treatment of Autonomic Failure in MSAP01NS044233 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LOW, PHILLIP A · 2003 to 2014
$12.4M
TRAFFICKING AND ABETA AGGREGATIONP01AG031097 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI KELLY, JEFFERY W · 2009 to 2013
$10.2M
Transgenic Models to Study Alzheimer's DiseaseR37AG011385 · NIA · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2002 to 2011
$4.9M
Project-002P30NS076411 · NINDS · SCINTILLON INSTITUTE FOR PHOTOBIOLOGY · PI LIPTON, STUART A · 2011 to 2016
$4.5M
TRANSGENIC MODELS TO SUDY ALZHEIMERS DISEASER01AG011385 · NIA · SCRIPPS RESEARCH INSTITUTE · PI MUCKE, LENNART · 1992 to 2017
$3.2M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
NIA NIH HHS AG022074NIA NIH HHS AG11385NIA NIH HHS AG18840NIA NIH HHS P01 AG010435NIA NIH HHS P01 AG022074NIA NIH HHS P01 AG031097NIA NIH HHS P50 AG005131NIA NIH HHS R01 AG011385NIA NIH HHS R37 AG011385NIA NIH HHS R37 AG018440NINDS NIH HHS NS044233NINDS NIH HHS P01 NS044233NINDS NIH HHS P30 NS076411
6 · The paper itself

Abstract

Progressive accumulation of α-synuclein (α-syn) in limbic and striatonigral systems is associated with the neurodegenerative processes in dementia with Lewy bodies (DLB) and Parkinson's disease (PD). The murine Thy-1 (mThy1)-α-syn transgenic (tg) model recapitulates aspects of degenerative processes associated with α-syn accumulation in these disorders. Given that axonal and synaptic pathologies are important features of DLB and PD, we sought to investigate the extent and characteristics of these alterations in mThy1-α-syn tg mice and to determine the contribution of α-syn c-terminally cleaved at amino acid 122 (CT α-syn) to these abnormalities. We generated a novel polyclonal antibody (SYN105) against the c-terminally truncated sequence (amino acids 121 to 123) of α-syn (CT α-syn) and performed immunocytochemical and ultrastructural analyses in mThy1-α-syn tg mice. We found abundant clusters of dystrophic neurites in layers 2 to 3 of the neocortex, the stratum lacunosum, the dentate gyrus, and cornu ammonis 3 of the hippocampus, striatum, thalamus, midbrain, and pons. Dystrophic neurites displayed intense immunoreactivity detected with the SYN105 antibody. Double-labeling studies with antibodies to phosphorylated neurofilaments confirmed the axonal location of full-length and CT α-syn. α-Syn immunoreactive dystrophic neurites contained numerous electrodense laminated structures. These results show that neuritic dystrophy is a prominent pathologic feature of the mThy1-α-syn tg model and suggest that CT α-syn might play an important role in the process of axonal damage in these mice as well as in DLB and PD.

Indexed as

AgedAged, 80 and overalpha-SynucleinAmino Acid SequenceAnimalsAntibodiesAntibody SpecificityAxonsBiomarkersDemographyDisease Models, AnimalFemaleHumansImmunohistochemistryLewy Body DiseaseMalealpha-SynucleinAntibodiesBiomarkersMutant ProteinsThy-1 Antigens

Identifiers

PMID23313024
PMCPMC3589076
OpenAlexW2025575563

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.