Evidence map›Paper›PMID 36138304›Full record

ArticleInflammopharmacology2022

Minocycline attenuates cholinergic dysfunction and neuro-inflammation-mediated cognitive impairment in scopolamine-induced Alzheimer's rat model.

Sabiheh Amirahmadi, Faezeh Dabouri Farimani, Mahsan Akbarian, Farshad Mirzavi, Mohammad Hossein Eshaghi Ghalibaf, Arezoo Rajabian, Mahmoud Hosseini

Abstract read
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In one paragraph

Article in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 12% 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, 28 citations in OpenAlex.

  1. Review
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  6. Article
  7. Doxycycline: An essential tool for Alzheimer's disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Review
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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 3 institutions in 1 country.

Sabiheh AmirahmadiPharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran.
Faezeh Dabouri FarimaniApplied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Mahsan AkbarianApplied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Farshad MirzaviCardiovascular Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran.
Mohammad Hossein Eshaghi GhalibafDepartment of Physiology, School of Medicine, Medical Department of Physiology, Tehran University of Medical Sciences, Tehran, Iran.
Arezoo RajabianDepartment of Internal Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. rajabianar@mums.ac.ir.ORCID http://orcid.org/0000-0003-3765-7463
Mahmoud HosseiniPsychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Hosseinim@mums.ac.ir.
Mashhad University of Medical Sciences · IRBirjand University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

National Institute for Medical Research Development 4000373
6 · The paper itself

Abstract

objectiveMinocycline, a semisynthetic tetracycline-derived antibiotic, has various pharmacological effect such as anti-inflammatory, anti-oxidative stress, and anti-apoptotic effects. The current study investigated the involvement of neuro-inflammatory, oxidative stress, and cholinergic markers in neuroprotection by minocycline against scopolamine-induced brain damage.

methodsMinocycline was administered (oral, 10, 15, and 30 mg/kg, daily) to groups of amnesic rats for 21 days. Passive avoidance memory and spatial learning and memory were assessed. Following that, oxidative stress, cholinergic function, and neuro-inflammation markers were evaluated in the brain tissue.

resultsAccording to our biochemical data, treatment of the scopolamine-injured rats with minocycline decreased the levels of malondialdehyde and acetylcholinesterase (AChE) as well as mRNA expression of AChE and neuro-inflammation markers (tumor necrosis factor-α, interleukin (IL)-1β, IL-6). It also increased the total thiol levels and superoxide dismutase activity as well as mRNA expression of cholinergic receptor M1 (ChRM1). Moreover, minocycline modified distance and latencies in Morris water maze, prolonged latency to enter the black zone and light time while decreasing time spent and frequency of entries to darkness.

conclusionTaken together, the data indicate that treatment with minocycline improved memory dysfunction mediated possibly through restoring AChE and ChRM1 levels, oxidant/antioxidant balance, as well as inhibiting inflammatory responses.

Indexed as

Alzheimer DiseaseCognitive DysfunctionMinocyclineAcetylcholinesteraseAnimalsCholinergic AgentsInflammationMaze LearningRatsRNA, MessengerScopolamineAcetylcholinesteraseCholinergic AgentsMinocyclineRNA, MessengerScopolamineAChECholinergic receptor M1Inflammatory responsePassive avoidance memorySpatial learning and memory

Identifiers

PMID36138304
OpenAlexW4296806999

What OpenQuestion holds

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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.