# Exploring the Effect of Genetic Testing on Personalised Treatment Plans for Depression

**Authors:** Shichao Li, Liang Peng, Yuting Wang

PMC · DOI: 10.62641/aep.v54i1.2098 · Actas Españolas de Psiquiatría · 2026-02-15

## TL;DR

This study shows that genetic testing for CYP2C19 can help tailor antidepressant treatment for depression, improving effectiveness and reducing side effects.

## Contribution

The study demonstrates how CYP2C19 metabolic typing can guide personalized antidepressant therapy for better outcomes.

## Key findings

- Patients with poor CYP2C19 metabolism (Group C) had better depression outcomes but more side effects.
- Intermediate metabolizers (Group B) showed better medication adherence compared to other groups.
- Rapid metabolizers (Group A) had the lowest adverse event rates but poorer treatment response.

## Abstract

As a result of individual genetic variations, some patients show no response to initial antidepressant medications. This study aims to investigate the association between specific genetic polymorphisms and the efficacy of antidepressant drugs and to improve the accuracy and effectiveness of treatment under the guidance of genetic testing.

A retrospective screening was conducted on medical records from, Suixian People's Hospital between January 2022 and December 2024. A total 202 patients with depression carrying the CYP2C19 gene were selected after the application of exclusion criteria. They were assigned to three groups in accordance with their genetic metabolism types: the rapid metabolism group (Group A, n = 65), the intermediate metabolism group (Group B, n = 94) and the poor metabolism group (Group C, n = 43). All three groups were treated with sertraline for a six-week treatment cycle. The observation indicators included scores on the Hamilton Depression Scale (HAMD); onset time of drug effect; rates of response and remission; scores on the Clinical Global Impression–Improvement (CGI–I) scale; levels of the neurotransmitter factors 5-hydroxytryptamine (5-HT), γ-aminobutyric acid (GABA) and brain-derived neurotrophic factor (BDNF); incidence of adverse events; and scores on the Morisky Medication Adherence Scale-8 (MMAS-8).

The baseline data of the three groups of patients were comparable before medication (p > 0.05). Compared with those in Groups A and B, patients in Group C showed a significantly greater reduction in HAMD scores (all p < 0.05), along with higher response rates (all p < 0.05) and remission rates (all p < 0.05). Amongst the three groups, Group C had a shorter onset time of drug effect (all p < 0.05); more significant improvement in CGI–I scores (all p < 0.05); and more prominent upregulation of neurotransmitter factors, namely, 5-HT (all p < 0.05), GABA (all p < 0.05) and BDNF (all p < 0.05). Regarding the incidence of adverse events, Group C had the highest rate, whereas Group A had the lowest (10.8% vs. 24.5% vs. 41.9%). Compared with other groups, Group B exhibited a more significant increase in MMAS-8 scores (all p < 0.05).

Metabolic phenotype exerts substantial effects on the therapeutic outcome of sertraline in patients with depression carrying the CYP2C19 gene. Amongst groups, Group C showed better therapeutic efficacy but an elevated incidence of adverse events and lower medication adherence; Group A had relatively poor efficacy; and Group B demonstrated superior adherence. In clinical practice, individualised treatment can be implemented on the basis of CYP2C19 metabolic typing to improve therapeutic efficacy and reduce adverse events and medical burden.

## Linked entities

- **Genes:** CYP2C19 (cytochrome P450 family 2 subfamily C member 19) [NCBI Gene 1557]
- **Chemicals:** sertraline (PubChem CID 68617), 5-hydroxytryptamine (PubChem CID 5202), γ-aminobutyric acid (PubChem CID 119)
- **Diseases:** depression (MONDO:0002050)

## Full-text entities

- **Genes:** BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, CYP2D6 (cytochrome P450 family 2 subfamily D member 6 (gene/pseudogene)) [NCBI Gene 1565] {aka CPD6, CYP2D, CYP2D7AP, CYP2D7BP, CYP2D7P2, CYP2D8P2}, CYP2C19 (cytochrome P450 family 2 subfamily C member 19) [NCBI Gene 1557] {aka CPCJ, CYP2C, CYPIIC17, CYPIIC19, P450C2C, P450IIC19}, NTF3 (neurotrophin 3) [NCBI Gene 4908] {aka HDNF, NGF-2, NGF2, NT-3, NT3}
- **Diseases:** bleeding (MESH:D006470), suicidal ideation (MESH:D001072), hypotension (MESH:D007022), neurological reactions (MESH:D009461), Comorbidity (MESH:D004194), shock (MESH:D012769), tension (MESH:D018781), HAMD (MESH:C538175), sleep disorders (MESH:D012893), pain (MESH:D010146), cyanosis (MESH:D003490), sexual  dysfunction (MESH:D012735), diabetes mellitus (MESH:D003920), insomnia (MESH:D007319), mental disorder (MESH:D001523), blood loss (MESH:D016063), anxiety (MESH:D001007), postpartum depression (MESH:D019052), Depression (MESH:D003866), Organic diseases (MESH:D000092124), nausea, vomiting (MESH:D020250), allergy (MESH:D004342), low (MESH:D009800), chronic diseases (MESH:D002908), coma (MESH:D003128), gastrointestinal bleeding (MESH:D006471), epilepsy (MESH:D004827), hypertension (MESH:D006973), Intellectual disability (MESH:D008607), gastrointestinal reactions (MESH:D005767), gastrointestinal adverse events (MESH:D002318), dizziness (MESH:D004244)
- **Chemicals:** GABA (MESH:D005680), alcohol (MESH:D000438), 5-HT (MESH:D012701), -aminobutyric  acid (MESH:D000613), Sertraline (MESH:D020280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12946719/full.md

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Source: https://tomesphere.com/paper/PMC12946719