# Modelling brain metabolism with interacting nonautonomous phase oscillators

**Authors:** Samuel J. K. Barnes, Anaí Echeverría, Joshua Hawley, Yevhen F. Suprunenko, Aneta Stefanovska

PMC · DOI: 10.3389/fnetp.2026.1720336 · Frontiers in Network Physiology · 2026-02-20

## TL;DR

This paper introduces a new model of brain metabolism using oscillators to study how metabolic processes synchronize and how their disruption might contribute to dementia.

## Contribution

The novel contribution is a nonautonomous phase oscillator model of neuronal energy metabolism that captures synchronization states without relying on detailed mass-based conservation laws.

## Key findings

- The model replicates key features of healthy neurovascular dynamics without empirical data fitting.
- Disruptions in metabolic synchrony are linked to dementia-related pathology.
- The framework allows for multiple synchronization states among metabolic processes.

## Abstract

Traditional brain models have focused primarily on electrical signalling, offering valuable insights but often overlooking the crucial role of metabolism within the neurovascular unit. Existing metabolic models tend to be highly detailed and mass-based, relying on strict conservation laws that limit their applicability to the brain’s thermodynamically open environment. In this study, we present a novel, phenomenological model of neuronal energy metabolism using a network of coupled Kuramoto oscillators. This nonautonomous phase dynamics framework captures complex, time-dependent interactions and allows for multiple synchronization states among metabolic processes. Our model captures key features consistent with healthy neurovascular dynamics, despite not being directly fitted to empirical data from resting-state brains and reveals how disruptions in metabolic synchrony may contribute to dementia-related pathology. By emphasizing the importance of metabolic coordination in the neurovascular unit, this work provides a versatile methodological foundation for future brain modelling efforts.

## Linked entities

- **Diseases:** dementia (MONDO:0001627)

## Full-text entities

- **Genes:** SLC16A1 (solute carrier family 16 member 1) [NCBI Gene 6566] {aka HHF7, MCT, MCT1, MCT1D}, SLC2A1 (solute carrier family 2 member 1) [NCBI Gene 6513] {aka CSE, DYT17, DYT18, DYT9, EIG12, GLUT}, SLC2A3 (solute carrier family 2 member 3) [NCBI Gene 6515] {aka GLUT3}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** neuronal damage (MESH:D009410), Dementia (MESH:D003704), type three diabetes (MESH:D003922), NVU (MESH:D013901), cardiovascular dysfunction (MESH:D002318), neuronal, metabolic, and vascular dysfunction (MESH:D002561), epilepsy (MESH:D004827), hypertension (MESH:D006973), Metabolic abnormalities (MESH:D008659), small vessel disease (MESH:D059345), cerebral hypoxia (MESH:D002534), stroke (MESH:D020521), functional hyperaemia (MESH:D003291), Huntington's (MESH:D006816), AD (MESH:D000544), neural dysfunction (MESH:D015441), central nervous system disorders (MESH:D002493), dementia with Lewy bodies (MESH:D020961), neurodegenerative disease (MESH:D019636), Chronic cerebral hypoperfusion (MESH:D006521), Parkinson's disease (MESH:D010300), mitochondrial dysfunction (MESH:D028361), autism spectrum disorder (MESH:D000067877)
- **Chemicals:** NADH (MESH:D009243), Glucose (MESH:D005947), ATP (MESH:D000255), GOa-MO (-), Glu (MESH:D018698), GABA (MESH:D005680), glycogen (MESH:D006003), lactate (MESH:D019344), pyruvate (MESH:D019289), oxygen (MESH:D010100)
- **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/PMC12969064/full.md

## References

102 references — full list in the complete paper: https://tomesphere.com/paper/PMC12969064/full.md

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Source: https://tomesphere.com/paper/PMC12969064