Evidence map›Paper›PMID 34958369›Full record

ArticleThe Journal of nutrition2022

Choline Supplementation Partially Restores Dendrite Structural Complexity in Developing Iron-Deficient Mouse Hippocampal Neurons.

Thomas W Bastian, William C von Hohenberg, Olivia R Kaus, Lorene M Lanier, Michael K Georgieff

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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  7. Molecules (Basel, Switzerland) · 2023
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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

5 authors at 1 institution in 1 country.

Thomas W BastianDepartment of Pediatrics, School of Medicine, University of Minnesota, Minneapolis, MN, USA.ORCID 0000-0001-5486-9471
William C von HohenbergDepartment of Pediatrics, School of Medicine, University of Minnesota, Minneapolis, MN, USA.
Olivia R KausDepartment of Pediatrics, School of Medicine, University of Minnesota, Minneapolis, MN, USA.
Lorene M LanierDepartment of Neuroscience, University of Minnesota, Minneapolis, MN, USA.
Michael K GeorgieffDepartment of Pediatrics, School of Medicine, University of Minnesota, Minneapolis, MN, USA.
University of Minnesota · US

Funding

NEWBORN IRON DEFICIENCYR01HD029421 · NICHD · UNIVERSITY OF MINNESOTA TWIN CITIES · PI GEORGIEFF, MICHAEL K. · 2000 to 2015
$4.4M
Impaired energy status and mitochondrial dynamics as causal factors for hippocampal neuron structuralabnormalities during developmental iron deficiencyF32HD085576 · NICHD · UNIVERSITY OF MINNESOTA · PI BASTIAN, THOMAS W. · 2016 to 2018
$166k
NICHD NIH HHS F32 HD085576NICHD NIH HHS R01 HD029421
6 · The paper itself

Abstract

backgroundFetal-neonatal iron deficiency causes learning/memory deficits that persist after iron repletion. Simplified hippocampal neuron dendrite structure is a key mechanism underlying these long-term impairments. Early life choline supplementation, with postnatal iron repletion, improves learning/memory performance in formerly iron-deficient (ID) rats.

objectivesTo understand how choline improves iron deficiency-induced hippocampal dysfunction, we hypothesized that direct choline supplementation of ID hippocampal neurons may restore cellular energy production and dendrite structure.

methodsEmbryonic mouse hippocampal neuron cultures were made ID with 9 μM deferoxamine beginning at 3 d in vitro (DIV). At 11 DIV, iron repletion (i.e., deferoxamine removal) was performed on a subset of ID cultures. These neuron cultures and iron-sufficient (IS) control cultures were treated with 30 μM choline (or vehicle) between 11 and 18 DIV. At 18 DIV, the independent and combined effects of iron and choline treatments (2-factor ANOVA) on neuronal dendrite numbers, lengths, and overall complexity and mitochondrial respiration and glycolysis were analyzed.

resultsCholine treatment of ID neurons (ID + Cho) significantly increased overall dendrite complexity (150, 160, 180, and 210 μm from the soma) compared with untreated ID neurons to a level of complexity that was no longer significantly different from IS neurons. The average and total length of primary dendrites in ID + Cho neurons were significantly increased by ∼15% compared with ID neurons, indicating choline stimulation of dendrite growth. Measures of mitochondrial respiration, glycolysis, and ATP production rates were not significantly altered in ID + Cho neurons compared with ID neurons, remaining significantly reduced compared with IS neurons. Iron repletion significantly improved mitochondrial respiration, ATP production rates, overall dendrite complexity (100-180 μm from the soma), and dendrite and branch lengths compared with untreated ID neurons.

conclusionsBecause choline partially restores dendrite structure in ID neurons without iron repletion, it may have therapeutic potential when iron treatment is not possible or advisable. Choline's mechanism in ID neurons requires further investigation.

Indexed as

IronIron DeficienciesAdenosine TriphosphateAnimalsCholineDeferoxamineDendritesDietary SupplementsHippocampusMiceNeuronsRatsAdenosine TriphosphateCholineDeferoxamineIronATPbrain developmentcholinedendritesenergy metabolismglycolysisiron deficiencymitochondrianeuron developmentoxidative phosphorylation

Identifiers

PMID34958369
PMCPMC8891184
OpenAlexW4200504465

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.