Salience network

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The salience network is theorized to mediate switching between the default mode network and central executive network.[1][2]

The salience network (SN) is a large scale brain network of the human brain that is primarily composed of the anterior insula (AI) and dorsal anterior cingulate cortex (dACC). It is involved in detecting and filtering salient stimuli, as well as in recruiting relevant functional networks.[3][4] Together with its interconnected brain networks, the SN contributes to a variety of complex functions, including communication, social behavior, and self-awareness through the integration of sensory, emotional, and cognitive information.[5]

The network is detectable through independent component analysis of resting state fMRI images, as well as seed based functional connectivity analysis. In addition to the AI and dACC, the salience network also consists of the substantia nigra, ventral tegmental area, ventral striatum, amygdala, dorsomedial thalamus, and hypothalamus. The functional connectivity has been linked with structural connectivity through diffusion tensor imaging, which reveals white matter tracts between the AI and dACC.


The salience network is primarily anchored at the AI and dACC. The node in the AI corresponds with the dorsal-anterior division distinguished in meta analyses of task-positive network related neuroimaging studies. The AI and dACC are linked via a white matter tract along the uncinate fasciculus. The subcortical nodes have yet to be structurally linked to the AI and dACC, however both seed based and resting state studies have observed intrinsic connectivity of the cortical nodes with subcortical nodes consisting of the sublenticular extended amygdala, the putamen, the dorsomedial thalamus, the ventral striatum, and the substantia nigra/ventral tegmental area.[6] The salience network is also distinguished by distinct cellular components, including von Economo neurons in the AI/dACC.[6] Cortico-striatal-thalamic loop circuits contribute to the salience network.[4]


While the function of the salience network is not exactly known, it has been implicated in the detection and integration of emotional and sensory stimuli, as well as in modulating the switch between the internally directed cognition of the default mode network and the externally directed cognition of the central executive network.[6] Evidence that the salience network mediates a switch between the DMN and CEN comes from granger causality analysis and studies utilizing transcranial magnetic stimulation.[7] The timing of electrophysiological responses during the oddball task is consistent with interaction, as after the initial mismatch negativity response is transmitted "bottom-up" from sensory regions, a "top-down" signal localized to the AI and dACC occurs before a widespread evoked potential that corresponds to attentional shifting.[3]


Dysfunction in the salience network have been observed in various psychiatric disorders, including anxiety disorders, post-traumatic stress disorder, schizophrenia, frontotemporal dementia, and Alzheimer's disease. The AI node of the salience network has been observed to be hyperactive in anxiety disorders, which is thought to reflect predictions of aversive bodily states leading to worrisome thoughts and anxious behaviors. In schizophrenia, both structural and functional abnormalities have been observed, thought to reflect excessive salience being ascribed to internally generated stimuli.[8] In individuals with autism, the relative salience of social stimuli, such as face, eyes, and gaze, may be diminished, leading to poor social skills.[5]


  1. ^ Sridharan, D.; Levitin, D. J.; Menon, V. (22 August 2008). "A critical role for the right fronto-insular cortex in switching between central-executive and default-mode networks". Proceedings of the National Academy of Sciences. 105 (34): 12569–12574. Bibcode:2008PNAS..10512569S. doi:10.1073/pnas.0800005105. PMC 2527952. PMID 18723676.
  2. ^ Nekovarova, Tereza; Fajnerova, Iveta; Horacek, Jiri; Spaniel, Filip (30 May 2014). "Bridging disparate symptoms of schizophrenia: a triple network dysfunction theory". Frontiers in Behavioral Neuroscience. 8: 171. doi:10.3389/fnbeh.2014.00171. PMC 4038855. PMID 24910597.
  3. ^ a b Menon, V; Uddin, LQ (June 2010). "Saliency, switching, attention and control: a network model of insula function". Brain Structure & Function. 214 (5–6): 655–67. doi:10.1007/s00429-010-0262-0. PMC 2899886. PMID 20512370.
  4. ^ a b Peters, SK; Dunlop, K; Downar, J (2016). "Cortico-Striatal-Thalamic Loop Circuits of the Salience Network: A Central Pathway in Psychiatric Disease and Treatment". Frontiers in Systems Neuroscience. 10: 104. doi:10.3389/fnsys.2016.00104. PMC 5187454. PMID 28082874.
  5. ^ a b Menon V. (2015) Salience Network. In: Arthur W. Toga, editor. Brain Mapping: An Encyclopedic Reference, vol. 2, pp. 597-611. Academic Press: Elsevier.
  6. ^ a b c Menon, V; Toga, A (2015). Salience Network. Elsevier. pp. 597–611. ISBN 978-0-12-397316-0.
  7. ^ Uddin, Lucina Q. (19 November 2014). "Salience processing and insular cortical function and dysfunction". Nature Reviews Neuroscience. 16 (1): 55–61. doi:10.1038/nrn3857. PMID 25406711.
  8. ^ Menon, V (October 2011). "Large-scale brain networks and psychopathology: a unifying triple network model". Trends in Cognitive Sciences. 15 (10): 483–506. doi:10.1016/j.tics.2011.08.003. PMID 21908230.