Hiring in life sciences? Share your open positions with our professional community. Read more Close

Advertisement

Sarcopenia in cognitive disorders: Toward a shared pathophysiological framework.

Created on 17 Sep 2026

Authors

Yiming Liu, Kah Hwei Clarice Chua, Clement Gwee You Qi, Jia Dong James Wang

Published in

Osteoporosis and sarcopenia. Volume 12. Issue 2. Pages 53-76. Epub May 07, 2026.

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.

PMID:
42369655
Bibliographic data and abstract were imported from PubMed on 17 Sep 2026.

Read full publication at:
Please sign in to see all details.

Advertisement

Stats

  • Community rating n/a 0 votes
  • Reviewers' rating n/a 0 votes
  • Your rating

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

  • Recommendations n/a n/a positive of 0 vote(s)
  • Views 6
  • Comments 0

Recommended by

  • No recommendations yet.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.

Advertisement