Evidence map›Paper›PMID 41962176›Full record

ReviewCurrent opinion in neurobiology2026

Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.

Gareth R Howell, Paul R Territo, David Aylor, Lee E Goldstein

Abstract readReview
In one paragraph

Review in Current opinion in neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

4 authors.

Gareth R HowellThe Jackson Laboratory, Bar Harbor, ME, 04609, USA; Graduate School of Biomedical Sciences, Tufts University, Boston, MA, USA; Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, USA. Electronic address: gareth.howell@jax.org.
Paul R TerritoStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA; Department of Medicine, Division of Clinical Pharmacology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA. Electronic address: pterrito@iu.edu.
David AylorCenter for Human Health and the Environment, Bioinformatics Research Center, Department of Biological Sciences, North Carolina State University, Raleigh, NC, 27695, USA. Electronic address: dlaylor@ncsu.edu.
Lee E GoldsteinBoston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, USA; Department of Neurology, Boston University School of Medicine, Boston, MA, USA; Department of Pathology, Boston University School of Medicine, Boston, MA, USA; Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA; Department of Ophthalmology, Boston University School of Medicine, Boston, MA, USA; Department of Biomedical Engineering, Boston University College of Engineering, Boston, MA, USA; Department of Electrical and Computer Engineering, Boston University College of Engineering, Boston, MA, USA. Electronic address: lgold@bu.edu.

Funding

Leveraging novel mouse models to investigate toxic metal exposures on brain aging and Alzheimer's diseaseU01AG088683 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LEE E. GOLDSTEIN, Gareth R Howell · 2024 to 2026
$6.2M
Impact of Toxic Metal Exposures in Novel Genetic Mouse Models of Late-Onset Alzheimer's DiseaseR56AG083940 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GOLDSTEIN, LEE E., HOWELL, GARETH R · 2023 to 2023
$823k
ICP-TOF Mass Spectrometer for Ultrafast Elemental Mapping of Clinical and Preclinical BiospecimensS10OD036450 · OD · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GOLDSTEIN, LEE E. · 2024 to 2024
$583k
Laser Ablation System for Ultrafast Elemental Mapping of Clinical and Preclinical BiospecimensS10OD038320 · OD · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GOLDSTEIN, LEE E. · 2025 to 2025
$316k
NIA NIH HHS R56 AG083940NIA NIH HHS U01 AG088683NIH HHS S10 OD036450NIH HHS S10 OD038320
6 · The paper itself

Abstract

Alzheimer's disease and related dementias (AD/ADRD) are modulated by gene-environment (GxE) interactions across the lifespan. Variants of specific genes increase AD risk and synergize with exposures to environmental toxicants ("exposome"), including neurotoxic metals and metalloids such as lead (Pb), cadmium (Cd), and arsenic (As). These neurotoxicants enter the body (via drinking water, contaminated food, and airborne particulates), transit in blood, cross the blood-brain barrier, and distribute in brain where the retained toxicant disrupts central nervous system development, structure, and function. Chronic exposure to these ubiquitous toxicants is common in disadvantaged communities, raising concerns about health risk disparities linked to geographic, socioeconomic, and racial demographics. While Pb, Cd, and As are established human neurotoxicants with suspected linkage to AD/ADRDs, the mechanisms underpinning AD/ADRD-related GxE interactions specific to metal-metalloid toxicant exposures are largely unknown and potentially modifiable. Preclinical models and resources are needed to facilitate research into the underlying mechanisms by which AD genetics and exposome affect brain health, aging, and AD/ADRD pathobiology.

Indexed as

Alzheimer DiseaseDementiaEnvironmental ExposureGene-Environment InteractionAnimalsBrainHumans

Identifiers

PMID41962176
PMCPMC13266488

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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.