Role of BDNF And IGF-1 in Aerobic and Resistance Exercise-Induced Neuroplasticity in Aging: A Narrative Review

Abstract Book of the 4th Global Conference on Aging and Gerontology

Year: 2026

[PDF]

Role of BDNF And IGF-1 in Aerobic and Resistance Exercise-Induced Neuroplasticity in Aging: A Narrative Review

Dr Subir Gupta, Ambadasu Bharatha, Md Anwarul Azim Majumder

ABSTRACT:

Neuroplasticity, the brain’s capacity to reorganize neural structure and function, declines progressively with advancing age, contributing to cognitive deterioration and increased vulnerability to neurodegenerative diseases. Among non-pharmacological interventions, physical exercise represents one of the most potent and scalable strategies for preserving brain health across the lifespan. Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) are principal mediators of exercise-induced neuroplasticity, exerting complementary and synergistic effects on neuronal survival, synaptic remodeling, neurogenesis, and cognitive function. This narrative review examines the sources and release patterns of BDNF and IGF-1 during aerobic and resistance exercise, analyzes the molecular signaling pathways underlying exercise-induced neuroplasticity, explores convergent and synergistic interactions between these neurotrophic factors, and evaluates their implications for cognitive preservation in aging. Aerobic exercise predominantly elevates BDNF through neuronal, endothelial, and platelet-related mechanisms, whereas resistance exercise more strongly stimulates systemic IGF-1 production via growth hormone-mediated hepatic release and skeletal muscle-derived mechano-growth factor. BDNF signals primarily through TrkB receptors, while IGF-1 acts through IGF-1 receptors, with both activating overlapping PI3K/Akt and MAPK/ERK cascades. Aging is characterized by parallel declines in BDNF and IGF-1 levels, reduced receptor expression, impaired downstream signaling due to neuroinflammation, and unfavorable shifts toward proBDNF and reduced IGF-1 sensitivity. Exercise restores this neurotrophic axis by co-elevating both factors through distinct but complementary pathways. Understanding the BDNF-IGF-1 axis provides a strong biological rationale for targeted exercise interventions aimed at lifelong cognitive preservation.

Keywords: Cognition; Receptors; Signaling Pathways; Neurogenesis; Long-Term Potentiation