# Diabetes mellitus is associated with an increased risk of postoperative neurocognitive disorders: a systematic review

**Authors:** Hong Li, Jing Xue, Zhiyong Gao, Li Xian, Jinlong Yuan, Jing He

PMC · DOI: 10.3389/fmed.2026.1726908 · Frontiers in Medicine · 2026-02-13

## TL;DR

People with diabetes are more likely to experience cognitive issues after surgery, and this review explores the connection and possible reasons behind it.

## Contribution

This study systematically reviews the association between diabetes and postoperative neurocognitive disorders, identifying key mechanisms and global research trends.

## Key findings

- Diabetes mellitus increases the risk of postoperative neurocognitive disorders by 1.84-fold.
- Key mechanisms include vascular brain injury, impaired glucose metabolism, inflammation, and oxidative stress.
- China, the USA, and Germany are leading research efforts on diabetes and cognitive outcomes after surgery.

## Abstract

Diabetes mellitus (DM) is increasingly recognized as an independent risk factor for perioperative neurocognitive disorders (PND). The rising global incidence of DM, projected to affect over 783 million people by 2045, necessitates a deeper understanding of its implications for surgical outcomes.

This review conducted a bibliometric analysis of 182 studies indexed in the Web of Science, focusing on the relationship between DM and PND. A systematic search was performed across multiple electronic databases, including PubMed and The Cochrane Library, to identify relevant articles published up to November 2024.

The analysis revealed that DM significantly increases the risk of PND, particularly POD, with studies indicating a 1.84-fold increased risk of POCD in diabetic patients. Key mechanisms identified include vascular brain injury, impaired glucose metabolism, inflammation, and oxidative stress. Notably, countries such as China, the USA, and Germany are leading research efforts in this area, highlighting a global interest in understanding these associations.

Further research is needed to elucidate causal mechanisms between DM and PND. Enhanced understanding of these mechanisms may inform targeted interventions to mitigate the risk of cognitive decline in diabetic patients undergoing surgery, ultimately improving patient outcomes and reducing healthcare burdens.

## Linked entities

- **Diseases:** Diabetes mellitus (MONDO:0005015)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, PDK1 (pyruvate dehydrogenase kinase 1) [NCBI Gene 5163], TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, SLC1A2 (solute carrier family 1 member 2) [NCBI Gene 6506] {aka DEE41, EAAT2, EIEE41, GLT-1, GLT1, HBGT}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, PIK3R1 (phosphoinositide-3-kinase regulatory subunit 1) [NCBI Gene 5295] {aka AGM7, GRB1, IMD36, p85, p85-ALPHA, p85alpha}, PDPK1 (3-phosphoinositide dependent protein kinase 1) [NCBI Gene 5170] {aka PDK1, PRO0461}, PTK2B (protein tyrosine kinase 2 beta) [NCBI Gene 2185] {aka CADTK, CAKB, FADK2, FAK2, PKB, PTK}, CAMK2B (calcium/calmodulin dependent protein kinase II beta) [NCBI Gene 816] {aka CAM2, CAMK2, CAMKB, CaMKIIbeta, MRD54}, JAK2 (Janus kinase 2) [NCBI Gene 3717] {aka JTK10}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}
- **Diseases:** impaired brain glucose metabolism (MESH:D044882), CAM (MESH:D020786), aortic dissection (MESH:D000784), DM (MESH:D003920), Mental Disorders (MESH:D001523), Alzheimer's disease (MESH:D000544), Hyperglycemia (MESH:D006943), POCD (MESH:D000079690), inflammation (MESH:D007249), HL (MESH:C538324), frailty (MESH:D000073496), metabolic disorder (MESH:D008659), delirium (MESH:D003693), obesity (MESH:D009765), POD (MESH:D000071257), diabetic retinopathy (MESH:D003930), PND (MESH:D019965), vascular brain injury (MESH:D020214), hypertension (MESH:D006973), brain injury (MESH:D001930), cognitive decline (MESH:D003072), type 1 (MESH:D003922), dementia (MESH:D003704), depression (MESH:D003866), type 2 DM (MESH:D003924)
- **Chemicals:** triglyceride (MESH:D014280), oxygen (MESH:D010100), blood glucose (MESH:D001786), STZ (MESH:D013311), isoflurane (MESH:D007530), metformin (MESH:D008687), Dexmedetomidine (MESH:D020927), TyG (-), glucose (MESH:D005947), LPS (MESH:D008070), CO2 (MESH:D002245)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

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## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12946032/full.md

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Source: https://tomesphere.com/paper/PMC12946032