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Abstract Background Apathy—a quantitative reduction of goal-directed activity—is among the most prevalent and disabling behavioral disturbances in neurodegenerative disease. Although traditionally treated as a non-specific neuropsychiatric symptom, accumulating evidence suggests that apathy reflects shared dysfunction of fronto-striatal motivation circuits and may operate as a transdiagnostic behavioral marker of brain disease, with implications for early detection, prognostication, and intervention. Objective To map the conceptualization, measurement, prevalence, neurobiology, prognostic significance, and treatment of apathy across major neurodegenerative diseases, and to identify priority gaps for psychological and behavioral science. Methods We conducted a scoping review following the Arksey and O’Malley framework as refined by the Joanna Briggs Institute methodology and reported in accordance with PRISMA-ScR. PubMed, Embase, PsycINFO, and the Cochrane Library were searched from inception to March 2026. Two reviewers independently screened 2,847 records at the title/abstract level, assessed 312 full-text articles, and charted data from 86 included studies using a structured extraction form. The selection process is presented in a PRISMA-ScR flow diagram (Fig. 1). Results Across diseases, pooled or representative prevalence estimates ranged from approximately 30% in MS and post-stroke cohorts to 49% in AD and up to 70% in bvFTD, with substantial variability driven by diagnostic instrument, disease stage, and care setting. Five conceptual frameworks dominated the literature: the Marin construct, the Levy–Dubois three-subtype model (cognitive, emotional-affective, auto-activation), the Robert et al. 2018 international consensus criteria, the Husain–Roiser transdiagnostic effort-based decision-making framework, and the Ismail Mild Behavioral Impairment (MBI) construct, which positions apathy as a prodromal marker of dementia. Neuroimaging consistently implicated anterior cingulate cortex, ventromedial and orbitofrontal cortex, ventral striatum, and their dopaminergic projections. Apathy independently predicted accelerated cognitive decline in AD and conversion from mild cognitive impairment to dementia, was associated with increased caregiver burden and reduced quality of life, and showed modest responsiveness to methylphenidate (Alzheimer’s disease) and to selected non-pharmacological strategies. Conclusions Apathy meets several criteria for a transdiagnostic behavioral marker: high prevalence, shared neurobiology, prognostic value, and partial treatment responsiveness. A psychology-informed research agenda—centered on dimensional measurement, ecologically valid behavioral tasks, and early-stage intervention—is needed to translate this construct into routine clinical practice and into preventive frameworks for cognitive decline.
Lin et al. (Thu,) studied this question.