Physical inactivity constitutes a measurable risk factor for neurodegeneration, with exercise triggering release of dozens of exerkines — bioactive proteins and metabolites including BDNF and VEGF — that directly engage neuroprotective mechanisms. Both moderate endurance training and targeted strength training stimulate these compounds, attenuating hippocampal atrophy and supporting neurogenesis, angiogenesis, and brain plasticity. The paper also draws an explicit link between exercise, neurodegeneration, and glaucoma, an underappreciated connection in sports medicine literature.
The exerkine framework is arguably the most consequential development in exercise neuroscience over the past decade. BDNF's role in hippocampal neurogenesis has been documented since the late 1990s, but cataloguing dozens of distinct exercise-released signaling molecules transforms exercise from a vague lifestyle recommendation into a pharmacologically-analogous intervention with identifiable molecular targets. For adults concerned with cognitive aging, this reframes the question from 'whether' to exercise to 'what type and dose' — with the evidence increasingly favoring combined endurance and resistance protocols over either alone. The glaucoma connection, while intriguing, requires more direct causal evidence. Critical limitations apply here: this appears to be a narrative review synthesizing existing intervention studies rather than presenting novel primary data, which limits causal confidence. Still, the synthesis is clinically actionable. For longevity-focused adults, the practical takeaway is unambiguous — sedentary behavior is not neurologically neutral, and even moderate structured exercise has measurable, mechanistically understood brain benefits.
