Narrative review: muscle-brain signaling in coexisting sarcopenia and cognitive impairment
This narrative review links sarcopenia with cognitive impairment in older adults and discusses endocrine, metabolic and exercise-related muscle-brain signaling as possible mechanisms; direct human pathway evidence remains limited. [1]
Automatic summary · not editorially reviewed
The key findings
Clinical evidence consistently links sarcopenia with cognitive impairment, and muscle strength and physical performance appear more closely related to cognitive function than muscle mass alone. [1]
The review names myokine and exerkine signaling, inflammaging, mitochondrial dysfunction, insulin resistance and lactate-mediated signaling as potential mechanisms. [1]
Direct evidence establishing complete signaling pathways in humans remains limited, according to the review. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- Older adults with sarcopenia and cognitive impairment, as discussed in a narrative review.
- Summary based on
- Study abstract
- Original publication
- September 16, 2026
Sarcopenia and cognitive impairment in older adults
The review addresses older adults, in whom sarcopenia and cognitive impairment frequently occur together. It reports that clinical evidence consistently links sarcopenia with cognitive impairment. It also states that muscle strength and physical performance appear more closely related to cognitive function than muscle mass alone. The authors frame this coexistence as possibly involving disrupted communication between skeletal muscle and the brain, in addition to shared age-related processes. These are described associations, not proof that one condition causes the other.
Supporting source [1]
Proposed endocrine and metabolic mechanisms
As potential mechanisms, the review names myokine and exerkine signaling, inflammaging and immune-endocrine dysregulation, mitochondrial dysfunction and oxidative stress, insulin resistance and glucose dysregulation, and lactate-mediated metabolic signaling. Exercise is described as a dynamic physiological context in which several components of muscle-brain communication can be modified, including inflammatory, metabolic, neurotrophic and lactate-related responses. These mechanisms are presented as potential explanations, not as established causal chains.
Supporting source [1]
Limited direct human pathway evidence
The review states that direct evidence establishing complete signaling pathways in humans remains limited. It calls for future studies that combine muscle and cognitive phenotypes with circulating biomarkers, metabolic measures and neuroimaging to clarify the clinical relevance of muscle-brain crosstalk in people with coexisting sarcopenia and cognitive impairment. Because this is a narrative review, its synthesis reflects the selected evidence rather than a systematic search.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a narrative review, so its synthesis reflects selected evidence rather than a systematic search. The proposed mechanisms are potential explanations, and direct evidence for complete signaling pathways in humans is described as limited. Associations do not establish causation.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Tian H, Huang L, Liu H, Li H, Zhao Y. · europepmc.org · September 16, 2026