ReviewGeroScience2026
Alzheimer's disease biomarkers in relation to non-cognitive domains within the intrinsic capacity framework: a narrative review.
Review in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) biomarkers may be associated with decline in non-cognitive domains of intrinsic capacity (IC), but such evidence has not been synthesized. This narrative review, based on a structured PubMed search (last search: December 31, 2025), included 119 human studies examining associations of core AD biomarkers (e.g., amyloid-beta (Aβ) and tau protein) and biomarkers of non-specific processes involved in AD pathophysiology (including neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), structural magnetic resonance imaging (MRI), and fluorodeoxyglucose positron emission tomography (FDG-PET)) with composite IC scores and non-cognitive IC domains. Among included studies, 2 investigated composite IC scores, 49 depressive symptoms, 30 locomotion, 29 hearing impairment, 19 vitality, and 1 vision impairment. The very limited longitudinal evidence on composite IC scores suggests that lower IC was associated with increased p-tau181 levels and that higher baseline NfL predicted steeper IC decline, whereas plasma Aβ42/Aβ40 showed no clear association. At the IC domains' level, higher cerebral Aβ deposition was associated with poorer locomotion, especially slower gait, more consistently than other biomarker modalities. Higher levels of tau biomarkers and NfL were more often associated with lower or declining handgrip strength. Depressive symptoms represented the most investigated non-cognitive IC domain, showing consistent longitudinal associations with lower fluid Aβ42, greater cerebral amyloid deposition, and subsequent brain atrophy. Hearing impairment was linked mainly to higher tau and NfL, reduced glucose metabolism, and brain atrophy; evidence for vision impairment was almost totally absent. Overall, the pattern of associations varied by biomarker modality, IC domain, and study design, suggesting that AD-related pathology and neurodegeneration have functional correlates beyond cognition. Methodological quality, formally appraised with the Newcastle-Ottawa Scale and the JBI checklist, was acceptable for most included studies.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.