Aged brain tissue suffers more histopathological damage following ischemia¹ and greater electrophysiological dysfunction following anoxia². In this short review, we consider the hypothesis that alterations in brain energy metabolism underlie age-related increases in brain vulnerability to anoxia, hypoxia, or ischemia (see also refs. 3–8). Investigations from our laboratories suggest that age-related decreases in the capacity of brain tissue to meet energy demand may limit recovery of ion homeostasis and excitability following large ion shifts or anoxia. These findings are consistent with earlier reports that glycolytic fluxes in rat brain during ischemia⁶ and glucose utilization during hyperthermia⁹ increased less with age and that resynthesis of depleted metabolic intermediates was slower in aged brains¹⁰. Such studies further suggest the hypothesis that age-related decreases in the capacity of brain tissue to match energy production to demand may limit recovery after metabolic insults.