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IGF-1

Insulin-like Growth Factor 1, Somatomedin C

Quick Stats
Studies 92
Trials 100
Score 3
2025 pubmed 1 citations

Mild Cognitive Impairment and Sarcopenia: Effects of Resistance Exercise Training on Neuroinflammation, Cognitive Performance, and Structural Brain Changes.

Oporto-Colicoi. Valeria V; Sepúlveda-Lara. Alexis A; Marzuca-Nassr. Gabriel Nasri GN; Sepúlveda-Figueroa. Paulina P

Key Findings

  • Resistance exercise activates the PI3K/Akt/mTOR pathway and increases IGF‑1, BDNF, and other neurotrophic factors.
  • Exercise shifts brain immune cells toward an anti‑inflammatory state, reducing neuroinflammation and supporting myelin health.
  • Older adults who do resistance training show better executive function, memory, and preserved gray‑matter volume in the hippocampus and precuneus, with effects lasting up to 18 months.

Practical Outcomes

  • Add a consistent resistance‑training routine (e.g., 2–3 sessions per week with progressive overload) to naturally boost IGF‑1 and support brain health. This non‑pharmacological approach can complement any IGF‑1 supplementation strategy and may help delay cognitive decline.

Summary

Doing regular resistance‑training workouts can raise your body’s own IGF‑1 and other brain‑helping proteins, cut brain inflammation, and improve memory and thinking in older adults with mild cognitive problems and muscle loss. The benefits can last for many months and even protect brain structures like the hippocampus.

Abstract

Mild cognitive impairment (MCI) and sarcopenia are prevalent age-related conditions that often coexist and share common mechanisms such as chronic inflammation, reduced neuroplasticity, and impaired muscle function. Resistance exercise training (RET) has emerged as a promising non-pharmacological strategy capable of addressing both physical and cognitive decline. The aim of this narrative review is to synthesize preclinical and clinical evidence on the effects of RET in older adults with MCI and sarcopenia, with a specific focus on its impact on neuroinflammation, cognitive performance and structural brain changes. At the molecular level, RET activates anabolic pathways, including PI3K/Akt/mTOR, enhances neurotrophic support via BDNF, NT-3, and IGF-1, and promotes hippocampal neurogenesis through exercise-induced myokines such as irisin and cathepsin B. RET also exerts immunomodulatory actions by shifting microglia toward anti-inflammatory M2 phenotypes, attenuating reactive astrogliosis, and supporting oligodendrocyte precursor cell differentiation, thereby improving myelin integrity. Neuroimaging studies consistently report preservation of hippocampal and precuneus gray matter, as well as improved white matter connectivity following RET. Clinically, RET has demonstrated significant and sustained improvements in executive function, memory, and global cognition, with effects persisting for up to 18 months. Collectively, RET represents a multifaceted intervention with the potential to delay progression from MCI to Alzheimer's disease by integrating neuroprotective, anti-inflammatory, and anabolic effects. Standardization of RET protocols and identification of biomarkers of responsiveness are needed to optimize its role within multimodal dementia-prevention strategies.

Study Information

Provider

pubmed

Year

2025

Date

2025-11-14T00:00:00.000Z

DOI

10.3390/ijms262211036

Citations

1

References

121