Evidence map›Paper›PMID 29691439›Full record

ArticleScientific reports2018

Reversal of memory and neuropsychiatric symptoms and reduced tau pathology by selenium in 3xTg-AD mice.

Ann Van der Jeugd, Arnaldo Parra-Damas, Raquel Baeta-Corral, Carlos M Soto-Faguás, Tariq Ahmed, Frank M LaFerla, Lydia Giménez-Llort, Rudi D'Hooge, Carlos A Saura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 51 citations in OpenAlex.

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  19. Social Nesting, Animal Welfare, and Disease Monitoring.Animals : an open access journal from MDPI · 2021
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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

9 authors at 4 institutions in 4 countries.

Ann Van der JeugdLaboratory of Biological Psychology, Katholieke Universiteit Leuven, Leuven, 3000, Belgium.ORCID 0000-0003-0916-248X
Arnaldo Parra-DamasInstitut de Neurociències, Departament de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain.ORCID 0000-0001-5683-060X
Raquel Baeta-CorralInstitut de Neurociències, Departament de Psiquiatria i Medicina Legal, Unitat de Psicologia Mèdica, Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain.
Carlos M Soto-FaguásInstitut de Neurociències, Departament de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain.
Tariq AhmedLaboratory of Biological Psychology, Katholieke Universiteit Leuven, Leuven, 3000, Belgium.
Frank M LaFerlaDepartment of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, 92697, CA, USA.
Lydia Giménez-LlortInstitut de Neurociències, Departament de Psiquiatria i Medicina Legal, Unitat de Psicologia Mèdica, Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain.
Rudi D'HoogeLaboratory of Biological Psychology, Katholieke Universiteit Leuven, Leuven, 3000, Belgium.
Carlos A SauraInstitut de Neurociències, Departament de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Bellaterra, 08193, Spain. carlos.saura@uab.es.
Universitat Autònoma de Barcelona · ESKU Leuven · BEHamad bin Khalifa University · QAUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulation of amyloid-β plaques and tau contribute to the pathogenesis of Alzheimer's disease (AD), but it is unclear whether targeting tau pathology by antioxidants independently of amyloid-β causes beneficial effects on memory and neuropsychiatric symptoms. Selenium, an essential antioxidant element reduced in the aging brain, prevents development of neuropathology in AD transgenic mice at early disease stages. The therapeutic potential of selenium for ameliorating or reversing neuropsychiatric and cognitive behavioral symptoms at late AD stages is largely unknown. Here, we evaluated the effects of chronic dietary sodium selenate supplementation for 4 months in female 3xTg-AD mice at 12-14 months of age. Chronic sodium selenate treatment efficiently reversed hippocampal-dependent learning and memory impairments, and behavior- and neuropsychiatric-like symptoms in old female 3xTg-AD mice. Selenium significantly decreased the number of aggregated tau-positive neurons and astrogliosis, without globally affecting amyloid plaques, in the hippocampus of 3xTg-AD mice. These results indicate that selenium treatment reverses AD-like memory and neuropsychiatric symptoms by a mechanism involving reduction of aggregated tau and/or reactive astrocytes but not amyloid pathology. These results suggest that sodium selenate could be part of a combined therapeutic approach for the treatment of memory and neuropsychiatric symptoms in advanced AD stages.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainDietary SupplementsDisease Models, AnimalFemaleHippocampusHumansMaze LearningMemoryMemory DisordersMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-PeptidesAmyloid beta-Protein PrecursorPresenilin-1Selenic AcidSeleniumtau Proteins

Identifiers

PMID29691439
PMCPMC5915484
OpenAlexW2799699068

What OpenQuestion holds

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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.