Evidence map›Paper›PMID 30220058›Full record

ArticleMolecular neurobiology2019

Choline Rescues Behavioural Deficits in a Mouse Model of Rett Syndrome by Modulating Neuronal Plasticity.

Eunice W M Chin, Wee Meng Lim, Dongliang Ma, Francisco J Rosales, Eyleen L K Goh

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. A lifespan staging model of basal forebrain cholinergic vulnerability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 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

5 authors at 3 institutions in 2 countries.

Eunice W M ChinNeuroscience Academic Clinical Programme, Duke-NUS Medical School, 20 College Road, Singapore, 169856, Singapore.
Wee Meng LimNeuroscience Academic Clinical Programme, Duke-NUS Medical School, 20 College Road, Singapore, 169856, Singapore.
Dongliang MaNeuroscience Academic Clinical Programme, Duke-NUS Medical School, 20 College Road, Singapore, 169856, Singapore.
Francisco J RosalesAbbott Nutrition Research and Development, Columbus, OH, USA.
Eyleen L K GohNeuroscience Academic Clinical Programme, Duke-NUS Medical School, 20 College Road, Singapore, 169856, Singapore. eyleen.goh@duke-nus.edu.sg.ORCID http://orcid.org/0000-0002-8244-6959
National University of Singapore · SGAbbott (United States) · USDuke-NUS Medical School · SG

Funding

GlaxoSmithKline Academic Center of Excellence Research AwardMinistry of Education - Singapore MOE2015-T2-1-022National Medical Research Council NMRC/CBRG/0094/2015National Research Foundation Singapore NRF 2008 NRF-CRP 002-082
6 · The paper itself

Abstract

Rett syndrome (RTT) is a postnatal neurodevelopmental disorder that primarily affects girls, with 95% of RTT cases resulting from mutations in the methyl-CpG-binding protein 2 (MECP2) gene. Choline, a dietary micronutrient found in most foods, has been shown to be important for brain development and function. However, the exact effects and mechanisms are still unknown. We found that 13 mg/day (1.7 × required daily intake) of postnatal choline treatment to Mecp2-conditional knockout mice rescued not only deficits in motor coordination, but also their anxiety-like behaviour and reduced social preference. Cortical neurons in the brains of Mecp2-conditional knockout mice supplemented with choline showed enhanced neuronal morphology and increased density of dendritic spines. Modelling RTT in vitro by knocking down the expression of the MeCP2 protein with shRNA, we found that choline supplementation to MeCP2-knockdown neurons increased their soma sizes and the complexity of their dendritic arbors. Rescue of the morphological defects could lead to enhanced neurotransmission, as suggested by an observed trend of increased expression of synaptic proteins and restored miniature excitatory postsynaptic current frequency in choline-supplemented MeCP2-knockdown neurons. Through the use of specific inhibitors targeting each of the known physiological pathways of choline, synthesis of phosphatidylcholine from choline was found to be essential in bringing about the changes seen in the choline-supplemented MeCP2-knockdown neurons. Taken together, these data reveal a role of choline in modulating neuronal plasticity, possibly leading to behavioural changes, and hence, a potential for using choline to treat RTT.

Indexed as

AnimalsBehavior, AnimalCerebral CortexCholineDendritic SpinesDietary SupplementsDisease Models, AnimalFemaleMethyl-CpG-Binding Protein 2Mice, KnockoutNeuritesNeuronal PlasticityPhosphatidylcholinesRats, Sprague-DawleyRett SyndromeCholineMethyl-CpG-Binding Protein 2PhosphatidylcholinesCholineNeurodevelopmentNutritionRett syndromeSynaptic plasticity

Identifiers

PMID30220058
PMCPMC6505515
OpenAlexW2891131058

What OpenQuestion holds

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LicenceCC BY
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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.