Evidence mapPaperPMID 41359280Full record

ArticleMolecular neurobiology2025

The Potential of Ectoine as a Brain Anti-Aging Agent in Rat Model of D-Galactose-Accelerated Aging May Be Mediated Through Crosstalk Between Redox/Mitochondrial Homeostasis/Autophagic/Apoptotic Pathways.

Aisha H A Alsenousy, Marwa B Bakir, Mohammed S Zommara, Hanan A Edres, Wael S Darwish, Rania M H M Eid, Maher A Kamel

Abstract read
In one paragraph

Article in Molecular neurobiology, 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

7 authors.

Aisha H A AlsenousyDepartment of Biochemistry, Medical Research Institute, University of Alexandria, 165 El-Horeya Rd, Al Ibrahimeyah Qebli WA Al Hadrah Bahri, Qesm Bab Sharqi, 21561, Alexandria, Egypt. aisha.ali@alexu.edu.eg.
Marwa B BakirMedical Education Department, Faculty of Medicine, Najran University, Najran, Saudi Arabia.
Mohammed S ZommaraDepartment of Internal Medicine, Faculty of Medicine, University of Alexandria, Alexandria, Egypt.
Hanan A EdresDepartment of Biochemistry, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt.
Wael S DarwishDepartment of Basic Science, College of Dentistry, Al Maaqal University, Al Basrah, 61003, Iraq.
Rania M H M EidDepartment of Physiology, Faculty of Medicine, Aswan University, Aswan, 81528, Egypt.
Maher A KamelDepartment of Biochemistry, Medical Research Institute, University of Alexandria, 165 El-Horeya Rd, Al Ibrahimeyah Qebli WA Al Hadrah Bahri, Qesm Bab Sharqi, 21561, Alexandria, Egypt. maher.kamel@alexu.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging has emerged as a prominent area of academic inquiry. Brain aging is a complex physiological process characterized by features such as enhanced apoptosis, oxidative stress, neuroinflammation, mitochondrial dysfunction, and impaired autophagy. Currently, effective preventative or therapeutic approaches for age-related neurodegenerative disorders remain elusive. Ectoine, a naturally occurring compatible solute, possesses diverse applications in biological engineering, cosmetics, medicine, and the food industry. Ectoine is reported to exhibit anti-inflammatory, antioxidant, and anti-apoptotic properties, making it a potential anti-aging agent. Consequently, the present study investigated the potential neuroprotective effects of Ectoine against D-galactose (D-gal)-induced brain aging. Accelerated aging was induced by subcutaneous injection of D-gal. Rats were subsequently divided into a control group, an aged group, and Ectoine-supplemented groups, receiving daily doses of 10, 20, and 40 mg/kg, respectively. Our findings revealed that Ectoine effectively and dose-dependently protected against D-gal-induced brain aging by inhibiting oxidative stress, enhancing the antioxidant system, decreasing neuroinflammation, restoring autophagy and mitochondrial homeostasis, and inhibiting apoptosis. Furthermore, Ectoine significantly restored the expression of miR-124 and its target genes; however, this effect is correlative and warrants further mechanistic validation. Additionally, while Ectoine's neuroprotective effects were observed at the tissue level, its cell-type specificity remains to be determined. These findings suggest that Ectoine may exert multi-pathway neuroprotective effects in brain aging. However, the current data are exploratory and warrant further validation to define causality and translational applicability.

Indexed as

AgingAmino Acids, DiaminoApoptosisAutophagyBrainGalactoseHomeostasisMitochondriaNeuroprotective AgentsAnimalsAntioxidantsDisease Models, AnimalMaleOxidation-ReductionOxidative StressRatsAmino Acids, DiaminoAntioxidantsectoineGalactoseNeuroprotective AgentsAgingApoptosisAutophagyD-galactoseEctoineMiR-124Mitochondrial homeostasisNeuroinflammationNeuroprotectionOxidative stress

Identifiers

PMID41359280
PMCPMC12686047

What Socratic 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 Socratic graph.