Lactate infusion fails to improve semantic categorization in Alzheimer's disease

Impaired neuronal energy metabolism, oxidative changes and microvascular abnormalities lead to altered lactate levels in Alzheimer's dementia. The aim of the present study was to assess whether intravenous sodium-lactate, a metabolic alternative and vasodilator that is thought to improve cognition, advances the cognitive performance of Alzheimer patients. Semantic categorization paradigm was used to present the electrophysiological correlates of natural scene categorization of Alzheimer patients before and after intravenous saline or sodium-lactate infusion. Mean amplitudes of event-related potentials (ERPs) were measured in two time windows before and after the treatments; two negative components (N1 between 150 and 250 ms and N2 between 400 and 600 ms) and one positive component (P2 between 250 and 400 ms) were identified. The negative components were more negative for the non-animal trials than for the animal trials while the positive component was similar for both categories. After the lactate treatment the amplitudes of the negative components became more negative mainly for the non-animal trials while the amplitude of the positive component turned more positive for the animal trials, however these changes were not significant. No changes have been observed after normal saline infusion. These results suggest that, contrary to its anticipated beneficial effects, sodium-lactate fails to significantly improve semantic categorization processes in Alzheimer's disease and this enhancement can be detected by recording ERPs. The effect of sodium-lactate to slightly improve semantic memory might be based on its positive effect on cardio- and cerebro-vascular function and neuronal metabolism.