Evidence map›Paper›PMID 40710964›Full record

ReviewToxics2025

Glutamate-Mediated Neural Alterations in Lead Exposure: Mechanisms, Pathways, and Phenotypes.

Wagner A Tamagno, Jennifer L Freeman

Abstract readReview
In one paragraph

Review in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Molecular and cellular mechanisms of lead-induced neurotoxicity: comparative insights from rodent and zebrafish models.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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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

2 authors.

Wagner A TamagnoSchool of Health Sciences, Purdue University, West Lafayette, IN 47907, USA.
Jennifer L FreemanSchool of Health Sciences, Purdue University, West Lafayette, IN 47907, USA.ORCID 0000-0002-3669-9111

Funding

Mechanisms of gene-environment interaction in developmental lead exposure leading to Alzheimer's disease phenotypesR01NS130722 · NINDS · PURDUE UNIVERSITY · PI Jennifer L. Freeman, Chongli Yuan · 2022 to 2026
$3.7M
Institute for a Sustainable Future NANIH HHS 1R01NS130722-02NINDS NIH HHS R01 NS130722
6 · The paper itself

Abstract

Lead (Pb) is a pervasive neurotoxicant with well-documented detrimental effects on the central nervous system, particularly in vulnerable populations such as children. Despite historical recognition of its toxicity, Pb exposure remains a significant public health concern due to its environmental persistence, historical industrial use, and ongoing applications in modern technologies. This review focuses on the mechanisms by which Pb disrupts glutamatergic signaling, a critical pathway for learning, memory, and synaptic plasticity. Pb's interference with glutamate receptors (ionotropic NMDA and AMPA, as well as metabotropic receptors), transporters (EAATs, VGLUTs, and SNATs), and metabolic pathways (glutamate-glutamine cycle, TCA cycle, and glutathione synthesis) are detailed. By mimicking divalent cations like Ca

Indexed as

calcium signalingEAATexcitotoxicityglutamateneurotoxicityNMDAPbsynaptic plasticity

Identifiers

PMID40710964
PMCPMC12300242

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.