Evidence map›Paper›PMID 34727320›Full record

ArticleBiological trace element research2022

The Role of Zinc Status on Spatial Memory, Hippocampal Synaptic Plasticity, and Insulin Signaling in icv-STZ-Induced Sporadic Alzheimer's-Like Disease in Rats.

Saltuk Bugra Baltaci, Omer Unal, Elif Gulbahce-Mutlu, Haluk Gumus, Suray Pehlivanoglu, Ahmet Yardimci, Rasim Mogulkoc, Abdulkerim Kasim Baltaci

Open access · greenAbstract read
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In one paragraph

Article in Biological trace element research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Neurochemical Research of LOXBlock-1 and ZnSOBiological trace element research · 2024
    Article
  7. Genetic deletion of zinc transporter ZnTFrontiers in molecular neuroscience · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

8 authors at 4 institutions in 1 country.

Saltuk Bugra BaltaciDepartment of Physiology, Medical Faculty, Selçuk University, Konya, 42031, Turkey.
Omer UnalDepartment of Physiology, Medical Faculty, Selçuk University, Konya, 42031, Turkey.
Elif Gulbahce-MutluDepartment of Medical Biology, Medical Faculty, KTO Karatay University, Konya, Turkey.
Haluk GumusDepartment of Neurology, Medical Faculty, Selçuk University, Konya, Turkey.
Suray PehlivanogluDepartment of Molecular Biology, Science Faculty, Necmettin Erbakan University, Konya, Turkey.
Ahmet YardimciDepartment of Physiology, Medical Faculty, Firat University, Elazig, Turkey.
Rasim MogulkocDepartment of Physiology, Medical Faculty, Selçuk University, Konya, 42031, Turkey.
Abdulkerim Kasim BaltaciDepartment of Physiology, Medical Faculty, Selçuk University, Konya, 42031, Turkey. baltaci61@yahoo.com.ORCID http://orcid.org/0000-0003-2461-1212
Selçuk University · TRFırat University · TRKTO Karatay University · TRNecmettin Erbakan University · TR

Funding

Scientific Research Projects Coordinatorship of Selcuk University 19102046
6 · The paper itself

Abstract

Alzheimer's disease (AD), especially its sporadic form (sAD), is of multifactorial nature. Brain insulin resistance and disrupted zinc homeostasis are two key aspects of AD that remain to be elucidated. Here, we investigated the effects of dietary zinc deficiency and supplementation on memory, hippocampal synaptic plasticity, and insulin signaling in intracerebroventricular streptozotocin (icv-STZ)-induced sAD in rats. The memory performance was evaluated by Morris water maze. The expression of hippocampal protein and mRNA levels of targets related to synaptic plasticity and insulin pathway was assessed by Western blot and real-time quantitative PCR. We found memory deficits in icv-STZ rats, which were fully recovered by zinc supplementation. Western blot analysis revealed that icv-STZ treatment significantly reduced hippocampal PSD95 and p-GSK3β, and zinc supplementation restored the normal protein levels. mRNA levels of BDNF, PSD95, SIRT1, GLUT4, insulin receptor, and ZnT3 were found to be reduced by icv-STZ and reestablished by zinc supplementation. Our data suggest that zinc supplementation improves cognitive deficits and rescues the decline in key molecular targets of synaptic plasticity and insulin signaling in hippocampus caused by icv-STZ induced sAD in rats.

Indexed as

Alzheimer DiseaseSpatial MemoryAnimalsDisease Models, AnimalHippocampusInsulinMaze LearningNeuronal PlasticityRatsRNA, MessengerStreptozocinZincInsulinRNA, MessengerStreptozocinZincAlzheimer’s diseaseBrain insulin resistanceLearning and memoryNeurodegenerationSynaptic plasticityZinc

Identifiers

PMID34727320
OpenAlexW3207995883

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.