Evidence map›Paper›PMID 30664867›Full record

ReviewJournal of molecular biology2019

Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation.

Tee Jong Huat, Judith Camats-Perna, Estella A Newcombe, Nicholas Valmas, Masashi Kitazawa, Rodrigo Medeiros

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 3 pooled it
29.6field-weighted citation impact, top 1% 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

192 citing papers in PubMed, 3 syntheses or guidelines pooled it, 455 citations in OpenAlex.

  1. Pooled it
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  4. Article
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  6. The Effects of CuSOBiology · 2026
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  18. Neurotoxic mechanisms of cadmium in neurodegenerative diseases.Frontiers in cell and developmental biology · 2026
    Review
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132 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

6 authors at 3 institutions in 2 countries.

Tee Jong HuatNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, Australia; Centre for Stem Cell Ageing and Regenerative Engineering, The University of Queensland, Brisbane, Australia. Electronic address: t.tee@uq.edu.au.
Judith Camats-PernaNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, Australia.
Estella A NewcombeNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, Australia.
Nicholas ValmasQueensland Brain Institute, The University of Queensland, Brisbane, Australia.
Masashi KitazawaCenter for Occupational and Environmental Health, Department of Medicine, University of California, Irvine, CA, USA.
Rodrigo MedeirosNeurula Laboratory, Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, Australia. Electronic address: rodrigo.medeiros@neurula.org.
University of Queensland · AUPark Centre for Mental Health · AUUniversity of California, Irvine · US

Funding

Environmental copper exposure and its impact on microglial Abeta clearanceR01ES024331 · NIEHS · UNIVERSITY OF CALIFORNIA, MERCED · PI KITAZAWA, MASASHI · 2014 to 2018
$2.7M
NIEHS NIH HHS R01 ES024331
6 · The paper itself

Abstract

As the median age of the population increases, the number of individuals with Alzheimer's disease (AD) and the associated socio-economic burden are predicted to worsen. While aging and inherent genetic predisposition play major roles in the onset of AD, lifestyle, physical fitness, medical condition, and social environment have emerged as relevant disease modifiers. These environmental risk factors can play a key role in accelerating or decelerating disease onset and progression. Among known environmental risk factors, chronic exposure to various metals has become more common among the public as the aggressive pace of anthropogenic activities releases excess amount of metals into the environment. As a result, we are exposed not only to essential metals, such as iron, copper, zinc and manganese, but also to toxic metals including lead, aluminum, and cadmium, which perturb metal homeostasis at the cellular and organismal levels. Herein, we review how these metals affect brain physiology and immunity, as well as their roles in the accumulation of toxic AD proteinaceous species (i.e., β-amyloid and tau). We also discuss studies that validate the disruption of immune-related pathways as an important mechanism of toxicity by which metals can contribute to AD. Our goal is to increase the awareness of metals as players in the onset and progression of AD.

Indexed as

AgingAluminumAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCadmiumDisease Models, AnimalEnvironmental ExposureGene Expression RegulationHumansInflammationLeadLife StylePhysical FitnessPresenilin-1tau ProteinsAluminumAmyloid beta-PeptidesCadmiumLeadMAPT protein, humanPresenilin-1PSEN1 protein, humantau Proteinsdementiaenvironmentneurodegenerationtauβ-amyloid

Identifiers

PMID30664867
PMCPMC6475603
OpenAlexW2909437563

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.