# A review of neurophysiological relationships between sleep disorders and depression

## TL;DR

This review explores how sleep disorders and depression share common neurophysiological mechanisms, offering insights into potential new treatments.

## Contribution

The paper introduces astrocytic dysfunction and GABA/glutamate imbalance as novel mechanisms linking sleep disorders and depression.

## Key findings

- Shared mechanisms include monoamine, HPA axis, and inflammatory factor dysregulation.
- Astrocytic dysfunction and GABA/glutamate imbalance reinforce pathological feedback loops.
- Treating sleep disorders may improve depression outcomes through shared therapeutic targets.

## Abstract

This review critically synthesizes current neurophysiological findings on the comorbidity between depression and sleep disorders. Drawing upon a multidisciplinary body of literature, the paper delineates overlapping neurochemical, hormonal, and inflammatory mechanisms. Further, it explores the role of astrocytic dysfunction and glutamate-GABA imbalance in reinforcing pathological feedback loops. By adopting an integrative framework, this review underscores the bidirectional and systemic nature of sleep disorder-depression comorbidity, offering insights into shared pathophysiological substrates and potential therapeutic targets for future research.

•The neurophysiological mechanisms of sleep-depression comorbidity are systematically reviewed.•A framework integrating monoamine, HPA axis, and inflammatory factor dysregulation is proposed.•Astrocytic dysfunction and GABA/glutamate imbalance are identified as key novel mechanisms.•Clarifying these shared targets provides direct pathways for novel therapeutic development.•Treating sleep disorders is posited as a viable strategy for improving depression outcomes.

The neurophysiological mechanisms of sleep-depression comorbidity are systematically reviewed.

A framework integrating monoamine, HPA axis, and inflammatory factor dysregulation is proposed.

Astrocytic dysfunction and GABA/glutamate imbalance are identified as key novel mechanisms.

Clarifying these shared targets provides direct pathways for novel therapeutic development.

Treating sleep disorders is posited as a viable strategy for improving depression outcomes.