Evidence map›Paper›PMID 32002777›Full record

ArticleCellular and molecular neurobiology2020

Neuroprotective Effects of Salidroside in a Mouse Model of Alzheimer's Disease.

Hualong Wang, Qiongqiong Li, Suya Sun, Shengdi Chen

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2020. 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
3.2field-weighted citation impact, top 7% 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, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Salidroside mitigates cognitive deficits in AlClFrontiers in behavioral neuroscience · 2026
    Article
  4. Review
  5. Article
  6. The EPMA journal · 2024
    Review
  7. Review
  8. Article
  9. The role of PI3K signaling pathway in Alzheimer's disease.Frontiers in aging neuroscience · 2024
    Review
  10. Review
  11. Phenolic Compounds ofInternational journal of molecular sciences · 2023
    Review
  12. Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 3 institutions in 1 country.

Hualong WangDepartment of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Qiongqiong LiDepartment of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Suya SunDepartment of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. sunsuya@shsmu.edu.cn.
Shengdi ChenDepartment of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. chensd@rjh.com.cn.
Shanghai Jiao Tong University · CNFirst Affiliated Hospital of Hebei Medical University · CNRuijin Hospital · CN

Funding

Innovation Program of Shanghai Municipal Education Commission 2017-01-07-00-01-E00046Natural Science Fund of China 91332107
6 · The paper itself

Abstract

Alzheimer's disease (AD), the most common form of dementia worldwide, is characterized by pathological hallmarks like β-amyloid peptide (Aβ) and clinical manifestations including cognitive impairment, psychiatry disorders, and behavioral changes. Salidroside (Sal) extracted from Rhodiola rosea L. showed protective effects against Aβ-induced neurotoxicity in a Drosophila AD model in our previous research. In the present study, daily doses of Sal were administered to APP/PS1 mice, a mouse model of AD, and several parameters were tested, including behavioral performance, Aβ status, levels of synapse-related proteins, and levels of PI3K/Akt targets of mTOR cell signaling pathway proteins. The behavioral testing showed an improvement in locomotor activity in the APP/PS1 mice after the administration of Sal. Treatment with Sal decreased both the soluble and insoluble Aβ levels and increased the expression of PSD95, NMDAR1, and calmodulin-dependent protein kinase II. The phosphatidylinositide PI3K/Akt/mTOR signaling was upregulated, which was in accordance with the above improvements from Sal treatment. Our findings suggested that Sal may protect the damaged synapses of the neurons in the APP/PS1 mice.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCognitive DysfunctionDisease Models, AnimalGlucosidesMice, Inbred C57BLMice, TransgenicNeuroprotective AgentsPhenolsPhosphatidylinositol 3-KinasesSignal TransductionTOR Serine-Threonine KinasesAmyloid beta-PeptidesGlucosidesNeuroprotective AgentsPhenolsPhosphatidylinositol 3-KinasesrhodiolosideTOR Serine-Threonine KinasesAlzheimer’s diseaseAmyloid-βNeuroprotectionPI3K/AktSalidroside

Identifiers

PMID32002777
PMCPMC11448871
OpenAlexW3003737770

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.