Evidence map›Paper›PMID 41075024›Full record

ArticleMetabolic brain disease2025

Protective and therapeutic effects of betanin nanoparticles in an alzheimer's rat model: modulation of behavior and expression of AQP4, BDNF, SIRT6, and Seladin-1.

Nasim Abedimanesh, Seyed Alireza Miri, Ali Mohammadi, Fatemeh Shahmohammadi, Hossein Danafar, Mohammad Reza Eskandari, Sajjad Hejazi, Sina Andalib, Behrooz Motlagh

Abstract read
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Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

9 authors.

Nasim AbedimaneshDepartment of Nutrition, School of Health, Zanjan University of Medical Sciences, Zanjan, Iran.ORCID 0000-0002-7254-9567
Seyed Alireza MiriDepartment of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran.
Ali MohammadiDepartment of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran.
Fatemeh ShahmohammadiDepartment of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran.
Hossein DanafarDepartment of Pharmaceutical Biomaterials, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran.ORCID 0000-0001-8956-7895
Mohammad Reza EskandariDepartment of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran.ORCID 0000-0001-6219-7185
Sajjad HejaziDepartment of Anatomy, Faculty of Veterinary Medicine, Near East University, Nicosia, Cyprus.
Sina AndalibDepartment of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran. andalibs@zums.ac.ir.ORCID 0000-0002-3744-7661
Behrooz MotlaghDepartment of Clinical Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran. b.motlagh@zums.ac.ir.ORCID 0000-0002-0837-0933

Funding

The Vice Chancellor for Research of Zanjan University of Medical Sciences, Zanjan, Iran A-12-898-19
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline, oxidative stress, and neuroinflammation. Betanin, a natural antioxidant, has shown neuroprotective potential, but its clinical use is limited by poor bioavailability. This study investigates the effects of betanin-loaded nanomicelles, designed to enhance brain delivery, in a scopolamine-induced rat model of AD. Nanomicelles were synthesized and characterized using TEM, DLS, and FT-IR. Rats received either pre- or post-treatment with betanin nanomicelles, free betanin, donepezil, or saline. Cognitive performance was assessed using the Morris Water Maze. Gene expression levels of AQP4, BDNF, SIRT6, and Seladin-1 were measured using real-time PCR, and antioxidant activity was evaluated by assessing glutathione (GSH) and glutathione reductase (GR) in hippocampal tissue. Betanin nanomicelles improved spatial memory, increased BDNF and SIRT6 expression, and reduced AQP4 levels, indicating potential neuroprotection. Seladin-1 expression was notably elevated in the pre-treatment group, suggesting support for neuronal survival. Antioxidant assays showed restoration of GSH and GR activity. These findings suggest that betanin nanomicelles may enhance cognitive function and modulate neuroprotective pathways more effectively than free betanin, supporting their potential as a novel therapeutic strategy for AD.

Indexed as

Alzheimer DiseaseAquaporin 4BetacyaninsBrain-Derived Neurotrophic FactorNanoparticlesNerve Tissue ProteinsNeuroprotective AgentsSirtuinsAnimalsAntioxidantsBehavior, AnimalDisease Models, AnimalHippocampusMaleMaze LearningMicrofilament ProteinsAntioxidantsAqp4 protein, ratAquaporin 4Bdnf protein, ratBetacyaninsbetaninBrain-Derived Neurotrophic FactorMicrofilament ProteinsNerve Tissue ProteinsNeuroprotective AgentsSirtuinsAlzheimer’s diseaseBetanin nanoparticlesCognitive functionNeuroprotectionOxidative stress

Identifiers

PMID41075024

What OpenQuestion holds

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Registered trials

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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.