# Moral decision-making in patients with neurodegenerative diseases: a systematic review

**Authors:** Giorgia Capitani, Daniele Lozzi, Giuseppe Curcio, Simone Migliore

PMC · DOI: 10.3389/fpsyg.2026.1745923 · Frontiers in Psychology · 2026-02-12

## TL;DR

This review explores how moral decision-making is affected in patients with different neurodegenerative diseases, linking impairments to specific brain network degeneration.

## Contribution

The study systematically identifies disease-specific patterns of moral cognition impairment in neurodegenerative disorders.

## Key findings

- bvFTD shows a utilitarian bias due to degeneration in the ventromedial prefrontal cortex and related networks.
- AD patients retain affective aversion to harm despite cognitive decline.
- PD and ALS show preserved moral reasoning unless frontotemporal involvement occurs.

## Abstract

Moral decision-making, a core component of social cognition, relies on integrating affective and cognitive processes supported by distributed neural networks. Neurodegenerative diseases disrupt these systems to varying degrees, offering unique models to investigate the neural bases of moral cognition. This review aimed to systematically examine moral decision-making deficits across neurodegenerative diseases, delineate disease-specific patterns of moral cognition impairment, and highlight conceptual and methodological gaps to inform future research and clinical assessment.

A systematic search of PubMed, Web of Science, and Scopus was conducted for studies published up to January 2025, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines.

Seventeen studies met inclusion criteria. Convergent evidence indicates that behavioral variant frontotemporal dementia (bvFTD) produces a distinctive utilitarian bias characterized by diminished empathy, emotional blunting, and impaired integration of intention and outcome, reflecting degeneration of the ventromedial prefrontal cortex, anterior insula, and amygdala within the salience and default mode networks. In contrast, Alzheimer’s disease (AD) patients typically preserve affective aversion to harm, suggesting relative sparing of limbic–ventromedial circuits despite conceptual and executive decline. Moral reasoning in Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) remains largely intact unless frontotemporal involvement occurs, while dementia with Lewy bodies (DLB) manifests intermediate profiles marked by reduced cognitive theory of mind and aberrant moral affect.

These findings delineate disease-specific patterns of moral dysfunction linked to network-level degeneration rather than global cognitive decline. Understanding these mechanisms holds translational relevance for early diagnosis, ethical capacity assessment, and the development of ecologically valid tools to monitor socio-emotional deterioration in neurodegenerative disorders.

## Linked entities

- **Diseases:** Alzheimer’s disease (MONDO:0004975), Parkinson’s disease (MONDO:0005180), amyotrophic lateral sclerosis (MONDO:0004976), dementia with Lewy bodies (MONDO:0007488)

## Full-text entities

- **Diseases:** non (MESH:C580335), impaired integration (MESH:D000081042), motor impairment (MESH:D000068079), memory impairment (MESH:D008569), Dopaminergic dysfunction (MESH:D009422), cognition deficits (MESH:D003072), -limbic dysfunction (MESH:D020363), cholinergic (MESH:C535672), rigidity (MESH:D009127), Moral dilemma (MESH:D013313), Deficits (MESH:D009461), behavioral dysregulation (MESH:D021081), FTD (MESH:D057180), Dementia (MESH:D003704), Parkinson (MESH:D010302), executive dysfunction (MESH:D006331), deficits in visuospatial and abstract reasoning (MESH:D000377), antisocial tendencies (MESH:C536965), slowed (MESH:D012897), lobes (MESH:D008878), neurodegenerative syndromes (MESH:D020271), impaired social-conceptual reasoning (OMIM:300082), degeneration (MESH:D009410), Amiotrophic Lateral Sclerosis (MESH:D016472), affective (MESH:D019964), DLB (MESH:D020961), aPCC atrophy (MESH:D001284), DL (MESH:C537113), neuropsychiatric (MESH:C000631768), subcortical-frontal impairments (MESH:D002544), attention and working memory deficits (MESH:D001289), psychotic (MESH:D011618), Behavioral disturbances (MESH:D001523), frontotemporal degeneration (MESH:D057174), diminished empathy (MESH:D015354), AD (MESH:D000544), aMCI (MESH:D060825), neurocognitive disorders (MESH:D019965), resting tremor (MESH:D014202), bradykinesia (MESH:D018476), Alzheimer's, frontotemporal, and Parkinson's disease (MESH:D010300), fronto-insular-temporal dysfunction (MESH:D017034), Intentionality comprehension (MESH:D001308), empathy loss (MESH:D016388), PFL (MESH:C536329), primary progressive aphasia (MESH:D018888), postural instability (MESH:D054972), ALS (MESH:D000690), ALS-FTD (OMIM:105550), Neurodegenerative diseases (MESH:D019636)
- **Chemicals:** dopamine (MESH:D004298)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

37 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935944/full.md

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Source: https://tomesphere.com/paper/PMC12935944