Evidence map›Paper›PMID 29203278›Full record

ArticleToxicology letters2018

Importance of tau in cognitive decline as revealed by developmental exposure to lead.

K Wright, S W Bihaqi, A Lahouel, A Masoud, F Mushtaq, A Leso, A Eid, N H Zawia

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Comparison of Blood Lead Levels in Patients With Alzheimer's Disease and Healthy People.American journal of Alzheimer's disease and other dementias · 2018
    Article
  4. 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

8 authors at 2 institutions in 2 countries.

K WrightDepartment of Cell and Molecular Biology, University of Rhode Island, Kingston Rhode Island, 02881, USA.
S W BihaqiGeorge and Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston Rhode Island, 02881, USA.
A LahouelDepartment of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston Rhode Island, 02881, USA.
A MasoudDepartment of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston Rhode Island, 02881, USA; Biochemical Technology Program, Faculty of Applied Science, Thamar University, Yemen.
F MushtaqDepartment of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston Rhode Island, 02881, USA.
A LesoInterdisciplinary Neuroscience Program, University of Rhode Island, Kingston Rhode Island, 02881, USA.
A EidDepartment of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston Rhode Island, 02881, USA; Interdisciplinary Neuroscience Program, University of Rhode Island, Kingston Rhode Island, 02881, USA.
N H ZawiaGeorge and Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston Rhode Island, 02881, USA; Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston Rhode Island, 02881, USA; Interdisciplinary Neuroscience Program, University of Rhode Island, Kingston Rhode Island, 02881, USA. Electronic address: nzawia@uri.edu.
University of Rhode Island · USThamar University · YE

Funding

Occupational exposure and the developmental-basis of ADR01ES015867 · NIEHS · UNIVERSITY OF RHODE ISLAND · PI ZAWIA, NASSER HUSSEIN · 2009 to 2012
$1.2M
A novel therapeutic approach to lowering tau and its impact on tauopathiesR21AG042695 · NIA · UNIVERSITY OF RHODE ISLAND · PI ZAWIA, NASSER HUSSEIN · 2013 to 2014
$408k
Neonatal exposure &neurodegeneration of the aged brainR03AG027246 · NIA · UNIVERSITY OF RHODE ISLAND · PI ZAWIA, NASSER HUSSEIN · 2005 to 2006
$121k
NIA NIH HHS R03 AG027246NIA NIH HHS R21 AG042695NIEHS NIH HHS R01 ES015867
6 · The paper itself

Abstract

Previous reports by us have determined that developmental exposure to the heavy metal lead (Pb) resulted in cognitive impairment in aging wildtype mice, and a latent induction in biomarkers associated with both the tau and amyloid pathways. However, the relationship between these two pathways and their correlation to cognitive performance needs to be scrutinized. Here, we investigated the impact of developmental Pb (0.2%) exposure on the amyloid and tau pathways in a transgenic mouse model lacking the tau gene. Cognitive function, and levels of intermediates in the amyloid and tau pathways following postnatal Pb exposure were assessed on young adult and mature transgenic mice. No significant difference in behavioral performance, amyloid precursor protein (APP), or amyloid beta (Aβ) levels was observed in transgenic mice exposed to Pb. Regulators of the tau pathway were impacted by the absence of tau, but no additional change was imparted by Pb exposure. These results revealed that developmental Pb exposure does not cause cognitive decline or change the expression of the amyloid pathway in the absence of tau. The essentiality of tau to mediate cognitive decline by environmental perturbations needs further investigation.

Indexed as

AgingAnimalsBehavior, AnimalBiomarkersBrainCognitive DysfunctionEnvironmental PollutantsFemaleHumansLeadMaleMice, Knockouttau ProteinsBiomarkersEnvironmental PollutantsLeadMAPT protein, humantau ProteinsAlzheimer’s diseaseAPPAβCDK5Lead (Pb)p35/25Tau knock-out mouse modelTau protein

Identifiers

PMID29203278
PMCPMC5803321
OpenAlexW2773649553

What OpenQuestion holds

Textmetadata
LicenceTDM
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.