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Intensive Care Unit Cognitive Disorders / Dementia and Cognitive Impairment Research · Journal article
Journal of Integrative Neuroscience · July 30, 2026
Encouraging direction, but not yet definitive.
This real-world observational study of 742 individuals across cognitive diagnostic groups reports significant associations between anticholinergic burden and depressive symptoms, multiple cognitive domains (short-term and long-term memory, working memory, attention, verbal fluency, reasoning), and functional performance. The authors emphasize that whilst associations are consistent, causal relationships cannot be inferred and minimizing anticholinergic burden is proposed as a pragmatic management strategy pending further research.
Observational cohort study with regression and clustering analyses. Individuals seeking care at the old-age psychiatry outpatient clinic of Patras University Mental Health Services, stratified by cognitive status.. Intervention: Anticholinergic burden (exposure; naturally occurring in clinical population). n = 742. Patras University Mental Health Services (Greece); single site..
Anticholinergic burden associated with depressive symptoms (coefficient 0.72, p < 0.001) Negative associations with short-term memory (–0.11, p = 0.017), long-term memory (–0.24, p < 0.001), working memory (–0.24, p = 0.001), attention/concentration (–0.13, p = 0.004) Negative association with verbal fluency (–0.57, p = 0.003) and inductive reasoning (–0.17, p = 0.002)
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These findings suggest that clinicians should consider minimizing anticholinergic burden in older patients with cognitive decline as a pragmatic strategy, particularly given the consistent associations across multiple cognitive domains, mood, and functional outcomes. However, the observational design precludes causal inference, and clinical decisions should await interventional evidence.
Observational study in real-world clinical setting demonstrates consistent associations between anticholinergic burden and multiple cognitive, functional, and mood domains across diagnostic groups, but cannot establish causation and lacks a comparator intervention.
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Quoted from the source exactly as published.
These findings suggest that clinicians should consider minimizing anticholinergic burden in older patients with cognitive decline as a pragmatic strategy, particularly given the consistent associations across multiple cognitive domains, mood, and functional outcomes. However, the observational design precludes causal inference, and clinical decisions should await interventional evidence.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background:Despite their negative effects on cognitive function and cognitive decline risk, drugs with anticholinergic properties are commonly prescribed, particularly in older individuals. In this observational study we aimed to shed light on the relationships between anticholinergic burden (ACB) and depressive symptoms and cognitive and functional performance in a real-world clinical setting. Methods:The study included individuals seeking care at the old-age psychiatry outpatient clinic of Patras University Mental Health Services. Depressive symptoms were assessed using the 15-item Geriatric Depression Scale; cognitive function was tapped using the Cognitive Telephone Screening Instrument, the Montreal Cognitive Assessment, and the Mini-Mental State Examination; and functional performance was assessed using the Bristol Activities of Daily Living Scale. Differences in demographic and clinical variables across the four diagnostic groups were analyzed. Regression analyses were performed to examine the associations between ACB, cognitive and non-cognitive symptoms, and demographic variables. In addition, clustering analyses were conducted to identify distinct, naturally occurring examinee subgroups and to assess if ACB differed across them. Results:The study sample consisted of individuals without cognitive impairment (N = 301), people with mild neurocognitive disorder (MiND, N = 264), major neurocognitive disorder caused by Alzheimer’s disease (ADMaND, N = 114), or other diseases (nonADMaND, N = 63). Significant associations were detected between ACB and depressive symptoms (0.72, p < 0.001), short-term memory (–0.11, p = 0.017), long-term memory (–0.24, p < 0.001), working memory (–0.24, p = 0.001), attention/concentration (–0.13, p = 0.004), verbal fluency (–0.57, p = 0.003), inductive reasoning (–0.17, p = 0.002), basic activities of daily living (0.29, p = 0.001), and instrumental activities of daily living (0.58, p < 0.001). The clustering analyses indicated that in the cluster including individuals with more advanced cognitive decline, poorer functional status, and more severe depressive symptoms, ACB was higher compared with the second group identified by the analyses (p < 0.001). Conclusions:ACB is related to different aspects of the clinical phenotype of cognitive decline. Despite the lack of solid evidence regarding causal relationships and need for further research, minimizing ACB in clinical settings may embody a potential pragmatic strategy in managing cognitive decline in ageing.
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