Evidence map›Paper›PMID 24454278›Full record

ArticleFrontiers in neuroscience2014

Novel autoimmune response in a tauopathy mouse model.

Carlos J Nogueras-Ortiz, Hector J De Jesús-Cortes, Jaime Vaquer-Alicea, Irving E Vega

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2014. 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
0.5field-weighted citation impact, top 34% 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, 8 citations in OpenAlex.

  1. Anti-IgLON5 Disease 10 Years Later: What We Know and What We Do Not Know.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Review
  2. 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 1 institution in 1 country.

Carlos J Nogueras-OrtizDepartment of Biology, University of Puerto Rico - Río Piedras Campus San Juan, PR, USA ; Department of Chemistry, University of Puerto Rico - Río Piedras Campus San Juan, PR, USA.
Hector J De Jesús-CortesDepartment of Biology, University of Puerto Rico - Río Piedras Campus San Juan, PR, USA.
Jaime Vaquer-AliceaDepartment of Biology, University of Puerto Rico - Río Piedras Campus San Juan, PR, USA.
Irving E VegaDepartment of Biology, University of Puerto Rico - Río Piedras Campus San Juan, PR, USA.
University of Puerto Rico at Río Piedras · PR

Funding

Upgrade Laboratories Facilities at UPR-Rio PiedrasR25GM061151 · NIGMS · UNIVERSITY OF PUERTO RICO RIO PIEDRAS · PI CARBALLEIRA, NESTOR MANUEL · 2001 to 2023
$32.5M
RIO PIEDRAS MARC U*STAR DEVELOPMENT PROGRAMT34GM007821 · NIGMS · UNIVERSITY OF PUERTO RICO RIO PIEDRAS · PI CARBALLEIRA, NESTOR MANUEL · 1985 to 2020
$20.3M
Neuroscience Research Opportunities to Increase Diversity (NeuroID)R25NS080687 · NINDS · UNIVERSITY OF PUERTO RICO RIO PIEDRAS · PI GARCIA-ARRARAS, JOSE E, MALDONADO-VLAAR, CARMEN SARA · 2012 to 2024
$5.3M
Autoimmune biomarker profiling in tauopathyR15NS081593 · NINDS · UNIVERSITY OF PUERTO RICO RIO PIEDRAS · PI VEGA, IRVING E · 2013 to 2013
$440k
NIGMS NIH HHS R25 GM061151NIGMS NIH HHS T34 GM007821NINDS NIH HHS R15 NS081593NINDS NIH HHS R25 NS080687
6 · The paper itself

Abstract

Molecular diagnostic tools with non-invasive properties that allow detection of pathological events in Alzheimer's disease (AD) and other neurodegenerative tauopathies are essential for the development of therapeutics. Several diagnostic strategies based on the identification of biomarkers have been proposed. However, its specificity among neurodegenerative disorders is disputable as the association with pathological events remains elusive. Recently, we showed that Amphiphysin-1 (AMPH1) protein's abundance is reduced in the central nervous system (CNS) of the tauopathy mouse model JNPL3 and AD brains. AMPH1 is a synaptic protein that plays an important role in clathrin-mediated endocytosis and associates with BIN1, one of the most important risk loci for AD. Also, it has been associated with a rare neurological disease known as Stiff-Person Syndrome (SPS). Auto-antibodies against AMPH1 are used as diagnostic biomarkers for a paraneoplastic variant of SPS. Therefore, we set up to evaluate the presence and abundance of auto-AMPH1 antibodies in tau-mediated neurodegeneration. Immunoblots and enzyme-linked immunosorbent assays (ELISA) were conducted to detect the presence of auto-AMPH1 antibodies in sera from euthanized mice that developed neurodegeneration (JNPL3) and healthy control mice (NTg). Results showed increased levels of auto-AMPH1 antibodies in JNPL3 sera compared to NTg controls. The abundance of auto-AMPH1 antibodies correlated with motor impairment and AMPH1 protein level decrease in the CNS. The results suggest that auto-AMPH1 antibodies could serve as a biomarker for the progression of tau-mediated neurodegeneration in JNPL3 mice.

Indexed as

Alzheimer's diseaseautoimmune responsebiomarkersdiagnosticstau-mediated neurodegenerationtauopathies

Identifiers

PMID24454278
PMCPMC3887318
OpenAlexW1990640976

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.