Evidence map›Paper›PMID 30632505›Full record

ArticleNeural regeneration research2019

Protective mechanism of testosterone on cognitive impairment in a rat model of Alzheimer's disease.

Xu-Sheng Yan, Zhan-Jun Yang, Jian-Xin Jia, Wei Song, Xin Fang, Zhi-Ping Cai, Dong-Sheng Huo, He Wang

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  15. Review
  16. [Testosterone and Alzheimer's disease].Problemy endokrinologii · 2022
    Article
  17. Article
  18. 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
  19. Impact of Testosterone on Alzheimer's Disease.The world journal of men's health · 2022
    Review
  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

8 authors at 2 institutions in 2 countries.

Xu-Sheng YanDepartment of Human Anatomy, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China.
Zhan-Jun YangDepartment of Human Anatomy, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China.
Jian-Xin JiaDepartment of Human Anatomy, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China.
Wei SongDepartment of Human Anatomy, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China.
Xin FangDepartment of Human Anatomy, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China.
Zhi-Ping CaiDepartment of Human Anatomy, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China.
Dong-Sheng HuoDepartment of Human Anatomy, Baotou Medical College, Baotou, Inner Mongolia Autonomous Region, China.
He WangSchool of Health Sciences, University of Newcastle, Newcastle, Australia.
Baotou Medical College · CNUniversity of Newcastle Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive dysfunction in Alzheimer's disease is strongly associated with a reduction in synaptic plasticity, which may be induced by oxidative stress. Testosterone is beneficial in learning and memory, although the underlying protective mechanism of testosterone on cognitive performance remains unclear. This study explored the protective mechanism of a subcutaneous injection of 0.75 mg testosterone on cognitive dysfunction induced by bilateral injections of amyloid beta 1-42 oligomers into the lateral ventricles of male rats. Morris water maze test results demonstrated that testosterone treatment remarkably reduced escape latency and path length in Alzheimer's disease rat models. During probe trials, testosterone administration significantly elevated the percentage of time spent in the target quadrant and the number of platform crossings. However, flutamide, an androgen receptor antagonist, inhibited the protective effect of testosterone on cognitive performance in Alzheimer's disease rat models. Nissl staining, immunohistochemistry, western blot assay, and enzyme-linked immunosorbent assay results showed that the number of intact hippocampal pyramidal cells, the dendritic spine density in the hippocampal CA1 region, the immune response and expression level of postsynaptic density protein 95 in the hippocampus, and the activities of superoxide dismutase and glutathione peroxidase were increased with testosterone treatment. In contrast, testosterone treatment reduced malondialdehyde levels. Flutamide inhibited the effects of testosterone on all of these indicators. Our data showed that the protective effect of testosterone on cognitive dysfunction in Alzheimer's disease is mediated via androgen receptors to scavenge free radicals, thereby enhancing synaptic plasticity.

Indexed as

Alzheimer's diseaseamyloid beta 1-42androgen receptorcognitive dysfunctionflutamidefree radicalsMorris water mazenerve regenerationneural regenerationneurodegenerative changepostsynaptic density protein 95synaptic plasticitytestosterone

Identifiers

PMID30632505
PMCPMC6352583
OpenAlexW2910398759

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.