Evidence map›Paper›PMID 29796989›Full record

ArticleMolecular neurobiology2019

Thyroid Hormone Supplementation Restores Spatial Memory, Hippocampal Markers of Neuroinflammation, Plasticity-Related Signaling Molecules, and β-Amyloid Peptide Load in Hypothyroid Rats.

Amina Chaalal, Roseline Poirier, David Blum, Serge Laroche, Valérie Enderlin

Abstract read
PubMed Publisher
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 37 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 3 pooled it
2.9field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 3 syntheses or guidelines pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. TMetabolic brain disease · 2026
    Article
  5. A study of the correlation between cognitive function and thyroid hormones in patients with Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Amina ChaalalNeuroscience Paris-Saclay Institute (Neuro-PSI), UMR 9197, CNRS, University Paris-Sud, University Paris-Saclay, F-91405, Orsay, France.
Roseline PoirierNeuroscience Paris-Saclay Institute (Neuro-PSI), UMR 9197, CNRS, University Paris-Sud, University Paris-Saclay, F-91405, Orsay, France.
David BlumInstitut National de la Santé et de la Recherche Medicale (INSERM), CHU-Lille, UMR-S 1172, Alzheimer and Tauopathies, LabEx DISTALZ, University Lille, F-59000, Lille, France.
Serge LarocheNeuroscience Paris-Saclay Institute (Neuro-PSI), UMR 9197, CNRS, University Paris-Sud, University Paris-Saclay, F-91405, Orsay, France.
Valérie EnderlinNeuroscience Paris-Saclay Institute (Neuro-PSI), UMR 9197, CNRS, University Paris-Sud, University Paris-Saclay, F-91405, Orsay, France. valerie.enderlin@u-psud.fr.ORCID http://orcid.org/0000-0002-8349-9059
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

Association France Alzheimer FADOC Convention tripartite France Alzheimer/FRC/ AAP 2013
6 · The paper itself

Abstract

Hypothyroidism is a condition that becomes more prevalent with age. Patients with untreated hypothyroidism have consistently reported symptoms of severe cognitive impairments. In patients suffering hypothyroidism, thyroid hormone supplementation offers the prospect to alleviate the cognitive consequences of hypothyroidism; however, the therapeutic value of TH supplementation remains at present uncertain and the link between cellular modifications associated with hypothyroidism and neurodegeneration remains to be elucidated. In the present study, we therefore evaluated the molecular and behavioral consequences of T3 hormone replacement in an animal model of hypothyroidism. We have previously reported that the antithyroid molecule propylthiouracil (PTU) given in the drinking water favors cerebral atrophy, brain neuroinflammation, Aβ production, Tau hyperphosphorylation, and altered plasticity-related cell-signaling pathways in the hippocampus in association with hippocampal-dependent spatial memory deficits. In the present study, our aim was to explore, in this model, the effect of hippocampal T3 signaling normalization on various molecular mechanisms involved in learning and memory that goes awry under conditions of hypothyroidism and to evaluate its potential for recovery of hippocampal-dependent memory deficits. We report that T3 supplementation can alleviate hippocampal-dependent memory impairments displayed by hypothyroid rats and normalize key markers of thyroid status in the hippocampus, of neuroinflammation, Aβ production, and of cell-signaling pathways known to be involved in synaptic plasticity and memory function. Together, these findings suggest that normalization of hippocampal T3 signaling is sufficient to reverse molecular and cognitive dysfunctions associated with hypothyroidism.

Indexed as

Signal TransductionAmyloid beta-PeptidesAnimalsAnxietyBehavior, AnimalBiomarkersHippocampusHypothyroidismMaleNeuronal PlasticityPropylthiouracilRats, WistarRNA, MessengerSpatial MemoryThyroid GlandThyroid HormonesAmyloid beta-PeptidesBiomarkersPropylthiouracilRNA, MessengerThyroid HormonesAmyloid peptideHippocampusHypothyroidismInflammationMemorySignaling pathways

Identifiers

PMID29796989
OpenAlexW2804675788

What OpenQuestion holds

Textmetadata
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.