Evidence map›Paper›PMID 28188358›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2017

Protective effect of valproic acid in streptozotocin-induced sporadic Alzheimer's disease mouse model: possible involvement of the cholinergic system.

Mirna Ezzat Sorial, Nesrine Salah El Dine El Sayed

Abstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Advances in the treatment of Alzheimer's disease.Frontiers in pharmacology · 2026
    Review
  4. Beyond epilepsy: The expanding role of valproic acid in Alzheimer disease therapy - a review.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Role of Cholinergic Signaling in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022
    Review
  14. Article
  15. A Mixture ofOxidative medicine and cellular longevity · 2022
    Article
  16. Article
  17. Article
  18. Article
  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

2 authors at 1 institution in 1 country.

Mirna Ezzat SorialDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Main Entrance of Al Tagamoa Al Khames, New Cairo City, 11835, Egypt.
Nesrine Salah El Dine El SayedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Main Entrance of Al Tagamoa Al Khames, New Cairo City, 11835, Egypt. nesrine_salah2002@yahoo.com.
German University in Cairo · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sporadic Alzheimer's disease (SAD) is a slowly progressive neurological disorder that is the most common form of dementia. Cholinergic system dysfunction and amyloid beta formation are the two main underlying pathological mechanisms for the disease development. In recent studies, insulin receptor desensitization and disturbances in the downstream effects of insulin receptor signaling were observed in the brains of Alzheimer's patients. Currently, intracereberoventricular (ICV) injection of streptozotocin (STZ) is found to induce behavioral, neurochemical, and structural alterations in animals resembling those found in SAD patients. Valproic acid (VPA), a histone deacetylase inhibitor (HDACi), was recently shown to regulate the transcription of several genes in both in vivo and in vitro models of Alzheimer's disease. The aim of the current study is to investigate the potential effect of different doses of valproic acid, in an ICV-STZ-induced animal model of SAD. Streptozotocin-injected mice showed cognitive and spatial memory dysfunction in the Y-maze, object recognition test, and Morris water maze (MWM) neurobehavioral tests. The mice also exhibited a decrease in acetylcholine (ACh) and neprilysin (NEP) levels accompanied by an increase in acetylcholinesterase (AChE) activity. For the first time to our knowledge, our findings have shown that VPA is capable of restoring ACh levels in ICV-STZ-injected mice, as well as normalizing both NEP levels and AChE activity. Via this mechanism, an enhancement of cognitive functions is observed. Thus, VPA is suggested to be a promising therapeutic approach against SAD.

Indexed as

AcetylcholineAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCognition DisordersDisease Models, AnimalDose-Response Relationship, DrugHistone Deacetylase InhibitorsMaleMaze LearningMemory DisordersMiceNeprilysinStreptozocinValproic AcidAcetylcholineAmyloid beta-PeptidesHistone Deacetylase InhibitorsNeprilysinStreptozocinValproic AcidAlzheimer’s diseaseCholinergic systemIntracerebroventricularStreptozotocinValproic acid

Identifiers

PMID28188358
OpenAlexW2586933678

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.