# Precision therapeutics in non-scarring alopecia: a systemic genomic and pathway-based framework for targeted interventions

**Authors:** Rinky Kapoor, Depti Bellani, Raji Patil, Debalina Bose, Madhuri Pola, Prashant Anilkumar Singh, Mamata Mishra, Debraj Shome

PMC · DOI: 10.5599/admet.3030 · ADMET & DMPK · 2025-12-16

## TL;DR

This paper proposes a precision medicine approach for non-scarring hair loss by combining genetic and pathway insights to guide targeted treatments.

## Contribution

It introduces a novel genomic and pathway-based framework for personalized interventions in androgenetic and alopecia areata.

## Key findings

- Androgenetic alopecia involves androgen-receptor signaling and inflammation, with finasteride as a key treatment.
- Alopecia areata is linked to immune dysregulation and responds well to JAK inhibitors.
- Regenerative therapies and AI diagnostics are emerging tools for personalized treatment.

## Abstract

Non-scarring alopecia, principally androgenetic alopecia and alopecia areata is highly prevalent and psychologically burdensome; androgenetic alopecia is androgen-driven, whereas alopecia areata is autoimmune. This review synthesizes genetic architecture and pathway biology to outline a precision framework for targeted interventions.

We reviewed full-text studies from the past decade across PubMed, Web of Science and Google Scholar, applying explicit inclusion/exclusion criteria; emphasis was placed on Genome wide association studies and Next generation sequencing findings, immune and androgen-axis biology, environmental modifiers, and therapeutic evidence (conventional, targeted, and regenerative), alongside artificial Intelligence-enabled diagnostics.

Androgenetic alopecia risk converges on androgen-receptor signalling and related loci, with perifollicular inflammation and oxidative stress as modifiers; finasteride remains a cornerstone therapy. Alopecia areata reflects polygenic immune dysregulation (e.g. Human leukocyte antigen/cytokine axes) with Janus Kinase-pathway inhibition yielding robust regrowth; across phenotypes, wingless-related integration sit/β-catenin and stem-cell programs are central targets. Regenerative options (Protein Rich Plasma, stem-cell/exosome approaches) and artificial Intelligence-assisted stratification are emerging adjuncts.

A pathway-guided, genotype and phenotype-informed strategy, targeting the androgen axis for androgenetic alopecia, immune circuits for alopecia areata, and adding regenerative or microenvironmental therapies where indicated-promises earlier diagnosis and more durable, individualized outcomes, especially as genome-wide association study/next-generation sequencing and artificial Intelligence tools are integrated into care.

## Linked entities

- **Proteins:** ctnnb1.S (catenin beta 1 S homeolog)
- **Chemicals:** finasteride (PubChem CID 57363)
- **Diseases:** androgenetic alopecia (MONDO:0005339), alopecia areata (MONDO:0004907)

## Full-text entities

- **Genes:** AR (androgen receptor) [NCBI Gene 367] {aka AIS, AR8, DHTR, HPCX3, HUMARA, HYSP1}, CTNNB1 (catenin beta 1) [NCBI Gene 1499] {aka CTNNB, EVR7, MRD19, NEDSDV, armadillo}
- **Diseases:** autoimmune (MESH:D001327), Alopecia areata (MESH:D000506), inflammation (MESH:D007249), Androgenetic alopecia (MESH:D000505)
- **Chemicals:** finasteride (MESH:D018120)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12994595/full.md

## References

106 references — full list in the complete paper: https://tomesphere.com/paper/PMC12994595/full.md

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Source: https://tomesphere.com/paper/PMC12994595