Evidence map›Paper›PMID 42563869›Full record

ReviewAnnals of the Child Neurology Society2025

Manganese Neurotoxicity and Familial Disorders of Manganese Transport.

Sidney M Gospe

Abstract readReview
In one paragraph

Review in Annals of the Child Neurology Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Sidney M GospeDepartments of Neurology and Pediatrics University of Washington Seattle Washington USA.ORCID https://orcid.org/0000-0002-0099-109X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Manganese is the 12th most common element in the Earth's crust and is an essential industrial component. Biologically, this metal plays an important role as a constituent of numerous enzymes. While manganese is required for normal biochemical and physiological processes, manganese excess can lead to significant toxicity, particularly to the central nervous system. Over the past 25 years, three inherited disorders of manganese transport have been described, leading to a model of how this essential metal is absorbed, distributed to tissues, and eliminated. The first part of this review describes the clinical features and cellular mechanisms of manganese toxicity due to occupational and environmental exposure. The remainder of the review discusses the familial disorder associated with hypomagnesemia, SLC39A8 deficiency, and the two genetic diseases resulting in hypermanganesemia, SLC30A10 deficiency and SLC39A14 deficiency. These latter two disorders are treatable, and the early recognition and institution of chelation therapy and iron supplementation can improve neurological disability. Ongoing research regarding the tissue-specific role of each transporter and their regulatory interplay, the varied mechanisms of manganese toxicity, and its treatment are also described.

Indexed as

hypermanganesemia dystonia 1hypermanganesemia dystonia 2manganeseSLC30A10SLC39A14SLC39A8

Identifiers

PMID42563869
PMCPMC13359167

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.