# Surface-based cortical thickness and gyrification mapping with data-driven prediction of cognitive impairment in prediabetes

**Authors:** Juan Wu, Qi Wang, Feifei Sun, Huiying Liao, Jinhong Song

PMC · DOI: 10.1016/j.ibneur.2026.02.013 · IBRO Neuroscience Reports · 2026-02-13

## TL;DR

This study finds that prediabetes is linked to brain changes in specific regions, which may predict cognitive decline using machine learning.

## Contribution

The study introduces a data-driven machine learning approach to predict cognitive impairment in prediabetes using cortical morphology.

## Key findings

- Prediabetes patients showed reduced cortical thickness in the left inferior temporal gyrus and decreased gyrification in the left precentral gyrus.
- Cortical thickness in the left ITG was negatively correlated with Trail Making Test Part B performance.
- Gradient Boosting classifier predicted cognitive impairment in prediabetes with high accuracy.

## Abstract

Prediabetes is a serious health condition characterized by blood glucose levels that are higher than normal but not high enough for a diagnosis of type 2 diabetes. It remains unclear whether alterations in cortical morphology occur during the prediabetic stage. This study aimed to investigate changes in cortical thickness and gyrification in individuals with prediabetes, and to explore whether these changes can predict cognitive performance using a machine learning approach.

T1-weighted MRI scans were acquired from 48 patients with prediabetes and 42 healthy controls. Surface-based morphometric analyses, including cortical thickness and the local gyrification index (LGI), were performed using FreeSurfer. Group comparisons were conducted. Neuropsychological assessments included the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA), and the Trail Making Test (TMT) Parts A and B. Pearson correlation analyses were conducted to examine associations between morphometric changes and cognitive performance. Furthermore, PyCaret, a machine learning framework, was applied to evaluate the predictive power of cortical features and clinical variables in predicting cognitive performance.

Compared with controls, individuals with prediabetes exhibited significantly reduced cortical thickness in the left inferior temporal gyrus (ITG) and decreased LGI in the left precentral gyrus. TMT-A and TMT-B scores were significantly higher in the prediabetes group, indicating poorer cognitive performance. Cortical thickness in the left ITG was negatively correlated with TMT-B performance (r = −0.54, 95 % CI: −0.71 to −0.31, p = 0.0001). Machine learning analysis identified the Extreme Gradient Boosting classifier as the best-performing model (AUC = 0.87, accuracy = 0.80).

Our findings suggest that cortical alterations in the ITG and precentral gyrus are evident during the prediabetic stage and relate to early cognitive dysfunction. These results highlight the potential of combining neuroimaging biomarkers and AI models for early detection and intervention in prediabetes-associated cognitive decline.

•Prediabetes patients had cortical thinning in the left inferior temporal gyrus and reduced gyrification in the left precentral gyrus.•Individuals with prediabetes exhibited impairments in processing speed and executive function.•Cortical thickness in the left inferior temporal gyrus negatively correlated with Trail Making Test Part B performance.•The Gradient Boosting classifier showed promise for early prediction of cognitive impairment in prediabetes populations.

Prediabetes patients had cortical thinning in the left inferior temporal gyrus and reduced gyrification in the left precentral gyrus.

Individuals with prediabetes exhibited impairments in processing speed and executive function.

Cortical thickness in the left inferior temporal gyrus negatively correlated with Trail Making Test Part B performance.

The Gradient Boosting classifier showed promise for early prediction of cognitive impairment in prediabetes populations.

## Linked entities

- **Diseases:** prediabetes (MONDO:0006920), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}
- **Diseases:** diabetes (MESH:D003920), ML (MESH:C537366), psychiatric disease (MESH:D001523), brain atrophy (MESH:C566985), AD (MESH:D000544), atrophy (MESH:D001284), Prediabetes (MESH:D011236), neurodegenerative diseases (MESH:D019636), neurological decline (MESH:D009461), stroke (MESH:D020521), IFG (MESH:D007003), insulin resistance (MESH:D007333), cerebrovascular disease (MESH:D002561), LGI (MESH:C566784), hypertension (MESH:D006973), structural brain abnormalities (MESH:D001927), brain injury (MESH:D001930), IGT (MESH:D018149), cognitive decline (MESH:D003072), organic disease (MESH:D000092124), T2DM (MESH:D003924)
- **Chemicals:** TGs (MESH:D014280), blood glucose (MESH:D001786), cholesterol (MESH:D002784), C-peptide (MESH:D002096), TC (-), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12927054/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12927054/full.md

## References

33 references — full list in the complete paper: https://tomesphere.com/paper/PMC12927054/full.md

---
Source: https://tomesphere.com/paper/PMC12927054