# Anomaly Detection for Structural and Functional Connectivity in Glioma Patients

**Authors:** Maria Colpo, Ryan Pollitt, Alexander Leemans, Diego Cecchin, Maurizio Corbetta, Alessandra Bertoldo, Alberto De Luca

PMC · DOI: 10.1002/nbm.70238 · 2026-03-10

## TL;DR

This study uses a machine learning model to detect brain connectivity changes in glioma patients by integrating structural and functional MRI data.

## Contribution

The novel use of variational autoencoders to integrate and detect anomalies in both structural and functional brain connectivity in glioma patients.

## Key findings

- Functional connectivity is more sensitive to changes distant from the tumor, while structural connectivity is more affected near the tumor.
- Abnormalities in functional connectivity align more closely with combined FC+SC changes than with structural connectivity alone.
- SC and FC impairments partially overlap within the tumor core but do not overlap in other brain regions.

## Abstract

Brain connectivity, quantified with diffusion MRI (structural connectivity, SC) and resting‐state functional MRI (functional connectivity, FC), can offer crucial insights into glioma‐brain network interactions. Currently, no standardized approach exists to integrate information from FC and SC and to identify potential tumor‐induced abnormalities at the single‐patient level. Variational autoencoders (VAEs) have been shown to be promising for learning the distribution of features representing a healthy brain and deviations thereof and can naturally be applicable to multiple modalities. This study explores the potential of VAE to integrate FC and SC and detect multimodal anomalies in brain connectivity in glioma patients. The VAE is trained on concatenated FC‐SC healthy data to learn how to reconstruct normative connectivity patterns. After ad hoc transfer learning, the model parameters are applied to the oncological dataset, to obtain the healthy version of the pathological matrices. Given the healthy, pathological, and reconstructed matrices, a statistic is developed with the goal of identifying specific alterations in SC, FC, and their FC + SC integration in glioma patients. SC, FC, and FC + SC abnormalities are compared with each other to explore their interplay and their link with tumor and surrounding brain tissues. Results show that FC is more sensitive to alterations distant from the tumor, while SC is more affected in its vicinity. Then, the alterations identified by FC are generally more in agreement with the alterations identified by FC + SC compared with those highlighted by SC. Moreover, SC abnormalities never overlap with FC + SC out of the tumor, and FC and SC single impairments partially overlap within the tumor core and never overlie in other brain tissues. This information could facilitate patient stratification, prognostic modeling, and personalized treatment planning.

Structural connectivity (SC) and functional connectivity (FC) provide crucial insights into glioma‐brain interactions. This study uses variational autoencoder to integrate FC and SC, detect anomalies, and investigate connectivity impairments in networks proximal and distal to the tumor.

## Linked entities

- **Diseases:** glioma (MONDO:0021042)

## Full-text entities

- **Genes:** F2R (coagulation factor II thrombin receptor) [NCBI Gene 2149] {aka CF2R, HTR, PAR-1, PAR1, TR}, SYNM (synemin) [NCBI Gene 23336] {aka DMN, SYN}, IDH1 (isocitrate dehydrogenase (NADP(+)) 1) [NCBI Gene 3417] {aka HEL-216, HEL-S-26, IDCD, IDH, IDP, IDPC}, NOS1 (nitric oxide synthase 1) [NCBI Gene 4842] {aka IHPS1, N-NOS, NC-NOS, NOS, bNOS, nNOS}
- **Diseases:** left hemisphere glioma (MESH:D002544), GD (MESH:D001037), Right Default A (MESH:C535682), HPC (MESH:C537243), death (MESH:D003643), Connectivity Impairments (MESH:D003240), brain lesion (MESH:D001927), necrosis (MESH:D009336), oncological (MESH:D000072716), cognitive impairments (MESH:D003072), neuropsychiatric or neurological disorders (MESH:D009422), Glioblastomas (MESH:D005909), brain tumor (MESH:D001932), depression (MESH:D003866), SC (MESH:D006450), psychiatric (MESH:D001523), Cancer (MESH:D009369), hemisphere lesions (MESH:D006832), disruptive behavior (MESH:D019958), Default B (MESH:D006509), edema (MESH:D004487), Glioma (MESH:D005910), neurological disorders (MESH:D009461), OI (MESH:C536030), damages (MESH:D020263), WM structural damage (MESH:D056784), SC abnormalities (MESH:C566527), connectomal diaschisis (MESH:D000087505), SC (MESH:D020914), Lesion (MESH:D009059), learning disabilities (MESH:D007859), SC anomalies (MESH:C536503), FC (MESH:D009372), stroke (MESH:D020521)
- **Chemicals:** BOLD (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12973340/full.md

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Source: https://tomesphere.com/paper/PMC12973340