The brain receives more information every second than it can possibly process. Some of it must be highlighted as relevant; most of it must be ignored. The job of detecting what matters falls largely to the salience network — a small but influential circuit centred on the anterior insula and dorsal anterior cingulate cortex. In schizophrenia, the salience network's failures may sit close to the heart of the disorder.
The salience network detects significant stimuli and coordinates switching between the default mode and executive networks; in schizophrenia, both detection and switching functions appear disrupted, providing a network-level account of the "aberrant salience" model of psychosis.
What the salience network is
The salience network was identified through resting-state fMRI in the mid-2000s, with William Seeley and Vinod Menon among its key descriptors. The core nodes are:
- The bilateral anterior insula — a region buried within the lateral sulcus, important for interoception (awareness of bodily states), emotional experience, and detecting behaviourally salient events.
- The dorsal anterior cingulate cortex (dACC) — central to cognitive control, conflict monitoring, and motivational signalling.
These regions are densely connected, share unique cell types (von Economo neurons), and act together to flag when something in the environment or body warrants a shift in attention.
The two roles of the salience network
1. Detecting salience
The salience network responds to events that are surprising, motivationally significant, or behaviourally relevant. These can be external (a sudden noise) or internal (a strong bodily sensation, a striking thought).
2. Switching between networks
Vinod Menon's triple network model proposes that the salience network acts as a switch, toggling between the default mode network (internally focused, self-referential) and the central executive network (externally focused, goal-directed). When something salient occurs, the salience network upweights the executive network and downweights the DMN. When nothing is happening, the DMN takes over.
Aberrant salience and psychosis
The "aberrant salience" model, articulated by Shitij Kapur in American Journal of Psychiatry (2003), proposes that psychosis arises when ordinary stimuli are inappropriately tagged as significant. A passing stranger feels charged with meaning. A song lyric seems written for the listener. The conscious mind constructs explanations for these salience signals, and those explanations become delusions. While Kapur's model emphasises striatal dopamine, the salience network is a natural neural substrate — the system that should have decided "this is not important" but failed to.
Functional imaging studies have consistently shown altered salience network activity in schizophrenia, with reduced activation to actually-salient stimuli and abnormal activation to neutral ones. Resting-state work suggests altered intra-network connectivity in the anterior insula and dACC.
Disrupted switching
Beyond salience detection, the salience network's switching role appears disrupted. Studies by Lena Palaniyappan, Sridharan and colleagues, and others have shown that the dynamic transitions between DMN and executive network — normally orchestrated by the salience network — are less efficient in schizophrenia. This may help explain:
- The intrusion of self-referential thought into goal-directed activity
- Difficulty disengaging from internal experience to attend to the external world
- Cognitive deficits that depend on rapid network reconfiguration
Insula structure and function
Structural MRI consistently shows reduced grey matter volume in the bilateral anterior insula in schizophrenia, with the anterior insula identified as one of the most reliably affected cortical regions in the ENIGMA Schizophrenia cortical analyses (2018, Molecular Psychiatry). The insula's role in interoception — awareness of internal bodily states — is particularly intriguing because disturbances of basic self-experience are a long-recognised feature of schizophrenia, sometimes summarised as "ipseity disturbance."
Salience network and antipsychotics
Antipsychotic treatment partially normalises some salience network abnormalities. Reduced striatal dopamine signalling, the main mechanism of antipsychotics, is thought to dampen aberrant salience signals downstream. This is a plausible biological correlate of the clinical observation that delusions and hallucinations gradually lose their grip on antipsychotics — not because memories disappear, but because the salience signals that kept them alive are reduced.
What the salience network story explains
The salience network framework helps integrate observations that previously seemed disconnected:
- Why ordinary events feel meaningful to people in early psychosis
- Why the boundary between self and world feels porous
- Why attention and cognitive control are impaired
- How striatal dopamine elevations may translate into the conscious experience of psychosis
What it does not explain
Salience network abnormalities are not specific to schizophrenia. They appear in autism, frontotemporal dementia, anxiety disorders, and depression. The salience network is sensitive to many forms of pathology. As with the DMN, its abnormality in schizophrenia is part of a distributed network problem rather than a unique signature.
Group-level findings about the salience network do not predict any individual person's brain or symptoms. Imaging is a research tool that informs theory; it is not a diagnostic test.
Implications for treatment
The salience network framework reinforces several familiar treatment ideas and suggests a few newer ones:
- Antipsychotics dampen aberrant salience signalling — this is consistent with their clinical effect.
- CBT for psychosis works in part by helping people re-evaluate the meaning of salient experiences. See our piece on CBTp.
- Mindfulness and interoceptive practices may modulate insula function, though this is an emerging area.
- Future biomarker work may use salience network connectivity as a treatment-response or risk-stratification tool, though clinical readiness is still some way off.
The bottom line
The salience network is a small circuit doing big work. It tells the brain what matters and helps switch between internally and externally focused modes. In schizophrenia, both functions are disrupted, providing a neural substrate for the aberrant salience model of psychosis and helping to explain how striatal dopamine elevations become conscious experience. Together with the default mode network and the central executive network, it forms the triple network whose dysfunction is increasingly central to how the field understands schizophrenia at the system level.
This article is for educational purposes only and is not medical advice, diagnosis, or treatment. Always consult a qualified mental health professional. If you or someone you know is in crisis, call or text 988 in the US, or your local emergency number.