Evidence map›Paper›PMID 29501530›Full record

ArticleNeurobiology of disease2018

Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease.

Qiu-Lan Ma, Edmond Teng, Xiaohong Zuo, Mychica Jones, Bruce Teter, Evan Y Zhao, Cansheng Zhu, Tina Bilousova, Karen H Gylys, Liana G Apostolova and 4 more

Abstract read
In one paragraph

Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

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  19. Review
  20. Synaptic Elimination in Neurological Disorders.Current neuropharmacology · 2019
    Review
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

14 authors.

Qiu-Lan MaDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States. Electronic address: QiulanMa@mednet.ucla.edu.
Edmond TengDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States.
Xiaohong ZuoDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States.
Mychica JonesDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States.
Bruce TeterDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States.
Evan Y ZhaoDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States.
Cansheng ZhuDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Department of Neurology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Tina BilousovaSchool of Nursing, University of California, Los Angeles, United States.
Karen H GylysSchool of Nursing, University of California, Los Angeles, United States.
Liana G ApostolovaDepartments of Neurology, Radiology, and Medical and Molecular Genetics, Indiana University School of Medicine, United States.
Mary Jo LaDuDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, United States.
Mir Ahamed HossainThe Johns Hopkins University School of Medicine, The Kennedy Krieger Institute, United States.
Sally A FrautschyDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States.
Gregory M ColeDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, United States; Veterans Affairs Greater Los Angeles Healthcare System, United States. Electronic address: GregoryCole@mednet.ucla.edu.

Funding

UCLA ALZHEIMERS DISEASE RESEARCH CENTERP50AG016570 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI APOSTOLOVA, LIANA G · 1999 to 2014
$25.9M
Preclinical Pharmacogenomics and Synaptic Biomarkers for Alzheimer's DiseaseR01AT006816 · NCCIH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COLE, GREGORY M, FRAUTSCHY, SALLY ANN · 2011 to 2015
$1.9M
Imaging and genetic biomarkers for Alzheimer's diseaseR01AG040770 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI APOSTOLOVA, LIANA G · 2012 to 2016
$1.4M
Imaging epigenetics of Alzheimer's DiseaseK02AG048240 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI APOSTOLOVA, LIANA G · 2014 to 2016
$434k
Modulation of tau pathogenesis by high dietary fat, gender and ApoE isoformR21AG050269 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FRAUTSCHY, SALLY ANN · 2016 to 2017
$347k
Curcumin and Yoga Exercise Effects in Veterans at Risk for Alzheimer's DiseaseI01RX000669 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI FRAUTSCHY, SALLY ANN · 2015 to 2015
–
Polyphenolic Interventions for tau Pathogenesis in Alzheimers ModelsI01BX001257 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI FRAUTSCHY, SALLY ANN · 2013 to 2016
–
Mechanisms for NSAID Alzheimer PreventionI01BX000542 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI COLE, GREGORY M · 2009 to 2013
–
BLRD VA I01 BX000542BLRD VA I01 BX001257BLRD VA I01 BX003485NCCIH NIH HHS R01 AT006816NIA NIH HHS K02 AG048240NIA NIH HHS P50 AG016570NIA NIH HHS R01 AG040770NIA NIH HHS R21 AG050269RRD VA I01 RX000669
6 · The paper itself

Abstract

Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). Apolipoprotein ε4 (APOE4) is the most common genetic risk factor for both familial AD (FAD) and sporadic AD; it accelerates Aβ aggregation and selectively impairs glutamate receptor function and synaptic plasticity. However, its molecular mechanisms remain elusive and these synaptic deficits are difficult to monitor. AD- and APOE4-dependent plasma biomarkers have been proposed, but synapse-related plasma biomarkers are lacking. We evaluated neuronal pentraxin 1 (NP1), a potential CNS-derived plasma biomarker of excitatory synaptic pathology. NP1 is preferentially expressed in brain and involved in glutamate receptor internalization. NP1 is secreted presynaptically induced by Aβ oligomers, and implicated in excitatory synaptic and mitochondrial deficits. Levels of NP1 and its fragments were increased in a correlated fashion in both brain and plasma of 7-8 month-old E4FAD mice relative to E3FAD mice. NP1 was also found in exosome preparations and reduced by dietary DHA supplementation. Plasma NP1 was higher in E4FAD+ (APOE4

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAnimalsBiomarkersBrainC-Reactive ProteinFemaleHumansMaleMiceMice, KnockoutNerve Tissue ProteinsPentraxinsSynapsesBiomarkersC-Reactive ProteinNerve Tissue ProteinsPentraxinsAlzheimer diseaseAPOEDementiaEFAD miceMCINeuronal pentraxin 1Plasma biomarkersβ-amyloid

Identifiers

PMID29501530
PMCPMC8092920

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.