Apathy as a failure of active inference
Apathy is common in neurological disorders, including dementias and conditions characterised by frontostriatal damage, where apathy is associated with faster progression and high caregiver burden.It has often been proposed that apathy results from changes in the cost–benefit analysis of decision-mak...
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| Veröffentlicht in: | Trends in neurosciences (Regular ed.) Jg. 48; H. 12; S. 940 - 951 |
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| Hauptverfasser: | , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
England
Elsevier Ltd
15.11.2025
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| Schlagworte: | |
| ISSN: | 0166-2236, 1878-108X, 1878-108X |
| Online-Zugang: | Volltext |
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| Zusammenfassung: | Apathy is common in neurological disorders, including dementias and conditions characterised by frontostriatal damage, where apathy is associated with faster progression and high caregiver burden.It has often been proposed that apathy results from changes in the cost–benefit analysis of decision-making. In effect, actions are said to become undesirable due to reward insensitivity or effort avoidance.Instead, we propose that apathy results from a failure of active inference, due to weak prior precision on action outcomes reducing the perceived discrepancy between the endpoints arising from action versus inaction. As a result, action becomes unnecessary, rather than being undesirable.Apathy correlates with prior precision on action outcomes. We propose that prior precision can be changed both behaviourally and pharmacologically, opening new avenues for the treatment of apathy.
Apathy is a common symptom across a wide range of neurodegenerative and psychiatric conditions, characterised by a loss of goal-directed action. It is associated with faster rates of cognitive and functional decline, poor prognosis, and high caregiver burden. Effective treatments remain elusive. In this article, we propose that apathy is not merely the result of actions becoming undesirable due to insufficient reward or an inflated sense of cost. Instead, actions become unnecessary due to a loss of prior precision on action outcomes in the context of the ‘Bayesian brain’. We outline the theoretical background and current evidence to support this framework and propose testable hypotheses regarding the behaviour, neuroanatomy, and neuropharmacology of apathy.
Apathy is a common symptom across a wide range of neurodegenerative and psychiatric conditions, characterised by a loss of goal-directed action. It is associated with faster rates of cognitive and functional decline, poor prognosis, and high caregiver burden. Effective treatments remain elusive. In this article, we propose that apathy is not merely the result of actions becoming undesirable due to insufficient reward or an inflated sense of cost. Instead, actions become unnecessary due to a loss of prior precision on action outcomes in the context of the ‘Bayesian brain’. We outline the theoretical background and current evidence to support this framework and propose testable hypotheses regarding the behaviour, neuroanatomy, and neuropharmacology of apathy. |
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| Bibliographie: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
| ISSN: | 0166-2236 1878-108X 1878-108X |
| DOI: | 10.1016/j.tins.2025.10.010 |