Evidence map›Paper›PMID 32477473›Full record

ArticleBasic and clinical neuroscience

Protective Role of Apigenin Against Aβ 25-35 Toxicity Via Inhibition of Mitochondrial Cytochrome c Release.

Farnaz Nikbakht, Yasaman Khadem, Sobhan Haghani, Hadiseh Hoseininia, Alireza Moein Sadat, Paria Heshemi, Nida Jamali

Open access · diamondAbstract read
In one paragraph

Article in Basic and clinical neuroscience. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
2.1field-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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

7 authors at 1 institution in 1 country.

Farnaz NikbakhtCellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-1239-3388
Yasaman KhademDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-2416-6999
Sobhan HaghaniDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-5993-0742
Hadiseh HoseininiaDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-4762-5756
Alireza Moein SadatDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-3282-4699
Paria HeshemiDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-2813-0803
Nida JamaliDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-2416-0335
Iran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCognitive dysfunction is the most common problem of patients with Alzheimer Disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss, synaptic dysfunction, and alteration in neurotransmitters receptors. Mitochondrial synapses dysfunction due to the accumulation of Amyloid Beta (Aβ) is one of the earliest pathological features of AD. The flavone apigenin has been reported to play some protective roles in AD through the anti-oxidative and anti-inflammatory properties. This study aimed at investigating the effects of apigenin on spatial working memory and neural protection by restoring mitochondrial dysfunction and inhibition of caspase 9.

methodsIntracerebroventricular (ICV) microinjection of Aβ 25-35 was used for AD modeling. Working memory was assessed 21 days later using the Y maze test. Neuronal loss was detected in the hilar area of the hippocampus using Nissl and Fluoro-jade B staining, whereas immunohistochemistry was used to illustrate cytochrome c positive cells and caspase 9.

resultsThe results revealed that apigenin significantly ameliorated spatial working memory. It also significantly reduced the number of degenerative neurons in the hilus area. Apigenin almost completely blocked the release of cytochrome c and caspase 9 in hilus.

conclusionApigenin may improve the spatial working memory deficits and neuronal degeneration through the amelioration of the mitochondrial dysfunction.

Indexed as

AlzheimerApigeninCytochrome cMemory

Identifiers

PMID32477473
PMCPMC7253805
OpenAlexW3004606536

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.