Evidence map›Paper›PMID 25045655›Full record

ArticleBioMed research international2014

Protective effects of testosterone on presynaptic terminals against oligomeric β-amyloid peptide in primary culture of hippocampal neurons.

Chi-Fai Lau, Yuen-Shan Ho, Clara Hiu-Ling Hung, Suthicha Wuwongse, Chun-Hei Poon, Kin Chiu, Xifei Yang, Leung-Wing Chu, Raymond Chuen-Chung Chang

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. [Testosterone and Alzheimer's disease].Problemy endokrinologii · 2022
    Article
  7. Prostate cancer treatment and the relationship of androgen deprivation therapy to cognitive function.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  8. Article
  9. Impact of Testosterone on Alzheimer's Disease.The world journal of men's health · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Prenatal Exposure to DEHP Induces Neuronal Degeneration and Neurobehavioral Abnormalities in Adult Male Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    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

9 authors at 5 institutions in 3 countries.

Chi-Fai LauLaboratory of Neurodegenerative Diseases, Department of Anatomy, LKS Faculty of Medicine, Room L1-49, 21 Sassoon Road, Pokfulam, Hong Kong.
Yuen-Shan HoLaboratory of Neurodegenerative Diseases, Department of Anatomy, LKS Faculty of Medicine, Room L1-49, 21 Sassoon Road, Pokfulam, Hong Kong ; State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau.
Clara Hiu-Ling HungLaboratory of Neurodegenerative Diseases, Department of Anatomy, LKS Faculty of Medicine, Room L1-49, 21 Sassoon Road, Pokfulam, Hong Kong ; Institute of Chinese Medicinal Science, University of Macau, Macau.
Suthicha WuwongseLaboratory of Neurodegenerative Diseases, Department of Anatomy, LKS Faculty of Medicine, Room L1-49, 21 Sassoon Road, Pokfulam, Hong Kong ; Department of Psychiatry, LKS Faculty of Medicine, Hong Kong.ORCID 0000-0002-4976-3514
Chun-Hei PoonLaboratory of Neurodegenerative Diseases, Department of Anatomy, LKS Faculty of Medicine, Room L1-49, 21 Sassoon Road, Pokfulam, Hong Kong.
Kin ChiuLaboratory of Neurodegenerative Diseases, Department of Anatomy, LKS Faculty of Medicine, Room L1-49, 21 Sassoon Road, Pokfulam, Hong Kong ; Department of Ophthalmology, LKS Faculty of Medicine, Hong Kong.
Xifei YangShenzhen Centre for Disease Control and Prevention, Shenzhen, China.
Leung-Wing ChuDivision of Geriatric, Department of Medicine, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, SAR, Hong Kong.ORCID 0000-0002-9066-2811
Raymond Chuen-Chung ChangLaboratory of Neurodegenerative Diseases, Department of Anatomy, LKS Faculty of Medicine, Room L1-49, 21 Sassoon Road, Pokfulam, Hong Kong ; Research Centre of Heart, Brain, Hormone and Healthy Aging, LKS Faculty of Medicine, Hong Kong ; State Key Laboratory of Brain and Cognitive Sciences, Hong Kong.ORCID 0000-0001-8538-7993
Chinese University of Hong Kong · HKMacau University of Science and Technology · MOShenzhen Center for Disease Control and Prevention · CNState Key Laboratory of Brain and Cognitive ScienceUniversity of Macau · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing lines of evidence support that testosterone may have neuroprotective effects. While observational studies reported an association between higher bioavailable testosterone or brain testosterone levels and reduced risk of Alzheimer's disease (AD), there is limited understanding of the underlying neuroprotective mechanisms. Previous studies demonstrated that testosterone could alleviate neurotoxicity induced by β-amyloid (Aβ), but these findings mainly focused on neuronal apoptosis. Since synaptic dysfunction and degeneration are early events during the pathogenesis of AD, we aim to investigate the effects of testosterone on oligomeric Aβ-induced synaptic changes. Our data suggested that exposure of primary cultured hippocampal neurons to oligomeric Aβ could reduce the length of neurites and decrease the expression of presynaptic proteins including synaptophysin, synaptotagmin, and synapsin-1. Aβ also disrupted synaptic vesicle recycling and protein folding machinery. Testosterone preserved the integrity of neurites and the expression of presynaptic proteins. It also attenuated Aβ-induced impairment of synaptic exocytosis. By using letrozole as an aromatase antagonist, we further demonstrated that the effects of testosterone on exocytosis were unlikely to be mediated through the estrogen receptor pathway. Furthermore, we showed that testosterone could attenuate Aβ-induced reduction of HSP70, which suggests a novel mechanism that links testosterone and its protective function on Aβ-induced synaptic damage. Taken together, our data provide further evidence on the beneficial effects of testosterone, which may be useful for future drug development for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApoptosisHippocampusHumansLetrozoleNeuronsNitrilesPresynaptic TerminalsPrimary Cell CultureProtective AgentsRatsTestosteroneTriazolesAmyloid beta-PeptidesLetrozoleNitrilesProtective AgentsTestosteroneTriazoles

Identifiers

PMID25045655
PMCPMC4086619
OpenAlexW1987465551

What OpenQuestion holds

Textmetadata
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.