ReviewOsteoporosis and sarcopenia2026
Sarcopenia in cognitive disorders: Toward a shared pathophysiological framework.
Review in Osteoporosis and sarcopenia, 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.
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Authors and funding
4 authors.
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Abstract
Sarcopenia and cognitive disorders frequently co-occur and may share convergent biology spanning systemic inflammation, vascular dysfunction, oxidative stress, and hormonal-metabolic dysregulation. Literature search was conducted using PubMed, Cochrane, Embase, and CENTRAL from January 2000 to March 2026. Search terms included "Sarcopenia", "Mild Cognitive Impairment", and "Dementia". Eighty-two studies met inclusion criteria (54 clinical; 28 interventions), discussing epidemiological trends, mechanistic pathways, biomarkers, and therapeutic targets. Clinical evidence clustered across inflammation, vascular change and energetics, hormonal-metabolic dysregulation, and biomarkers. Elevated inflammatory mediators tracked slower gait, weaker grip, and poorer cognition, mapping to mobility decline and Montreal Cognitive Assessment (MoCA) deficits. Cross-domain readouts linked muscle and brain: muscular fat infiltration related to worse cognitive-motor performance; temporalis muscle thickness correlated with MoCA and tau signal; impaired post-exercise phosphocreatine recovery associated with higher neurodegeneration risk and slower processing/gait. Blood biomarkers consistently stratified motor-cognitive status/decline. Among intervention reports, aerobic/resistance training improved strength, mobility, and often processing outcomes; protein (± vitamin D) and n-3 polyunsaturated fatty acid showed supportive but heterogeneous effects; vitamin D alone showed mixed muscle results but associated with lower dementia incidence; single-pathway metabolic/anti-cytokine strategies were mixed. Few studies powered dual musculoskeletal-cognitive endpoints, limiting quantitative synthesis. There is compelling evidence for bidirectional crosstalk between sarcopenia and cognitive impairment. However, evidence substantiating shared interventions remains limited and could benefit from more multi-center dual-outcome randomized controlled trials. Establishing consensus risk stratification criteria based on common biomarkers may support integrated management of these conditions, improving patient outcomes.
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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 Socratic graph.