Investigation of the Potential Neuroprotective Mechanisms of <i>Acalypha indica</i> Against Alzheimer's Disease by Integrated Bioinformatics Analysis.

Overview

1. Institute of Theoretical and Applied Research, Duy Tan University, Hanoi 100000, Vietnam
2. College of Medicine and Pharmacy, Duy Tan University, Da Nang 550000, Vietnam
3. Cancer Research Program, Department of Medicine, McGill University Health Center, Montreal, QC H4A3J1, Canada
4. College of Health Sciences, Vin University, Hanoi 100000, Vietnam
5. Vinmec International Hospital, Hanoi 100000, Vietnam

Abstract

Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders; however, available treatments majorly offer symptomatic relief without delaying disease progression and are associated with various adverse effects, highlighting the need for development of alternative therapies. Acalypha indica has previously showed neuroprotective effects in aging-related animal models, yet its mechanisms against AD were not fully understood. In this study, we employed an integrated bioinformatics approach combining network pharmacology, transcriptomic analysis, and molecular docking to investigate the anti-AD potential of this herb. A total of 282 overlapping targets between A. indica compounds and AD were identified. Network pharmacology analysis indicated chrysin, daidzein, galangin, kaempferol, and quercetin as the key bioactive components. Enrichment analyses suggested that targets of these compounds are mainly associated with phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) and mitogen-activated protein kinase (MAPK) signaling pathways. Protein–protein interaction (PPI) analysis identified AKT1, epidermal growth factor receptor (EGFR), interleukin 6 (IL6), tumor necrosis factor (TNF), and p53 protein (TP53) as crucial hub targets. These targets were significantly upregulated in AD brain samples and were closely associated with pathways related to neurodegeneration, inflammation, as well as alterations in immune cell infiltration. Among the compounds, quercetin exhibited the strongest binding affinity to these target proteins. Overall, these findings provide a strong foundation for the multi-target therapeutic potential of A. indica in AD.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

• geo:GSE33000, at NCBI GEO; found in the text, “2.4. Expression and Diagnostic Performance of…”

Data Availability Statement

The raw data supporting the conclusions of this article will be made available by the authors on request.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 3 authors, 7 keywords, 12 MeSH terms, 79 references.

Cite

This paper

Nguyen, L. T. H., Nguyen, H. T., & Nguyen, T. U. (2026). Investigation of the Potential Neuroprotective Mechanisms of <i>Acalypha indica</i> Against Alzheimer's Disease by Integrated Bioinformatics Analysis. International journal of molecular sciences, 27(14), 6196. https://doi.org/10.3390/ijms27146196

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.3390/biomedicines14050998 [code]

Integrative Multi-Omics and Machine Learning Analysis Identifies Therapeutic Targets and Drug Repurposing Candidates for Alzheimer's Disease.

Journal: Biomedicines

In common: NCBI GEO GSE33000, Alzheimer's / dementia, genetics / omics, cellular / molecular, 2 references

[2] doi:10.1186/s12967-026-08385-7

Dihydrotanshinone I as a novel signal transducer and activator of transcription 3 inhibitor for glioblastoma treatment.

Journal: Journal of translational medicine

In common: cellular / molecular, 5 references

[3] doi:10.1038/s41419-026-08791-1

The PM20D1-OLE pathway induces microglia rewiring to ameliorate Alzheimer disease.

Journal: Cell death & disease

In common: NCBI GEO GSE33000, Alzheimer's / dementia, genetics / omics, cellular / molecular, 1 reference

[4] doi:10.3390/metabo16080541

Spatial Metabolomics and Single-Cell Virtual Knockout Screening Reveal Solanesol Improves Parkinson's Disease-like Pathology Based on Lipid Inflammation Mechanism.

Journal: Metabolites

In common: genetics / omics, cellular / molecular, 4 references

[5] doi:10.3389/fimmu.2026.1937738

Multi-regional transcriptomic analysis reveals early nociceptive and neuroinflammatory alterations in APP/PS1 mice.

Journal: Frontiers in immunology

In common: NCBI GEO GSE33000, Alzheimer's / dementia, genetics / omics, cellular / molecular

[6] doi:10.3389/fnins.2026.1837233

Integrated multi-omics and deep learning analysis reveals neurotransmitter metabolism regulatory mechanisms of Tianwang Buxin Dan.

Journal: Frontiers in neuroscience

In common: genetics / omics, cellular / molecular, 4 references

[7] doi:10.3390/cimb48040369

Elucidating the Multi-Target Anti-Pruritic Mechanism of <i>Polygonatum odoratum</i> via Integrated Network Pharmacology, Molecular Simulations, and GEO Dataset Validation.

Journal: Current issues in molecular biology

In common: cellular / molecular, 4 references

[8] doi:10.1016/j.apsb.2026.04.017

PYGL-driven glycogenolysis impairs microglial autophagic flux <i>via</i> SNAP29 <i>O</i>-GlcNAcylation in Alzheimer's disease.

Journal: Acta pharmaceutica Sinica. B

In common: NCBI GEO GSE33000, Alzheimer's / dementia, cellular / molecular

[9] doi:10.1186/s12916-026-04957-y [code]

Thyroid-stimulating hormone receptor mediates peripheral-central neuroimmune crosstalk in autoimmune thyroid diseases.

Journal: BMC medicine

In common: genetics / omics, cellular / molecular, 3 references

[10] doi:10.1080/19490976.2026.2693397 [code]

Gut <i>Proteobacteria</i> glycine metabolism regulates neuroplasticity, motivation, and reinstatement of cocaine self-administration in mice.

Journal: Gut microbes

In common: genetics / omics, cellular / molecular, 3 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.