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Publication - A lactate-dependent shift of glycolysis mediates synaptic and cognitive processes in male mice by Fernandez-Moncada, I., G. Lavanco, U. B. Fundazuri, N. Bollmohr, S. Mountadem, T. Dalla Tor, P. Hachaguer, F. Julio-Kalajzic, D. Gisquet, R. Serrat, L. Bellocchio, A. Cannich, B. Fortunato-Marsol, Y. Nasu, R. E. Campbell, F. Drago, C. Cannizzaro, G. Ferreira, A. K. Bouzier-Sore, L. Pellerin, J. P. Bolanos, G. Bonvento, L. F. Barros, S. H. R. Oliet, A. Panatier and G. Marsicano, Nat Commun
Abstract
Astrocytes control brain activity via both metabolic processes and gliotransmission, but the physiological links between these functions are scantly known. Here we show that endogenous activation of astrocyte type-1 cannabinoid (CB1) receptors determines a shift of glycolysis towards the lactate-dependent production of d-serine, thereby gating synaptic and cognitive functions in male mice. Mutant mice lacking the CB1 receptor gene in astrocytes (GFAP-CB1-KO) are impaired in novel object recognition (NOR) memory. This phenotype is rescued by the gliotransmitter d-serine, by its precursor l-serine, and also by lactate and 3,5-DHBA, an agonist of the lactate receptor HCAR1. Such lactate-dependent effect is abolished when the astrocyte-specific phosphorylated-pathway (PP), which diverts glycolysis towards l-serine synthesis, is blocked. Consistently, lactate and 3,5-DHBA promoted the co-agonist binding site occupancy of CA1 post-synaptic NMDA receptors in hippocampal slices in a PP-dependent manner. Thus, a tight cross-talk between astrocytic energy metabolism and gliotransmission determines synaptic and cognitive processes.
Publication - Neuroprotective effects of lactate and ketone bodies in acute brain injury by Plourde, G., H. Roumes, L. Suissa, L. Hirt, E. Doche, L. Pellerin, A. K. Bouzier-Sore and H. Quintard, J Cereb Blood Flow Metab
Abstract :
The goal of neurocritical care is to prevent and reverse the pathologic cascades of secondary brain injury by optimizing cerebral blood flow, oxygen supply and substrate delivery. While glucose is an essential energetic substrate for the brain, we frequently observe a strong decrease in glucose delivery and/or a glucose metabolic dysregulation following acute brain injury. In parallel, during the last decades, lactate and ketone bodies have been identified as potential alternative fuels to provide energy to the brain, both under physiological conditions and in case of glucose shortage. They are now viewed as integral parts of brain metabolism. In addition to their energetic role, experimental evidence also supports their neuroprotective properties after acute brain injury, regulating in particular intracranial pressure control, decreasing ischemic volume, and leading to an improvement in cognitive functions as well as survival. In this review, we present preclinical and clinical evidence exploring the mechanisms underlying their neuroprotective effects and identify research priorities for promoting lactate and ketone bodies use in brain injury.
Keywords: Alternative brain fuels; TBI; brain metabolism; hypoxia; ketone bodies; lactate; neuroprotection; stroke.
Publication - Whole-brain T2 mapping with radial sampling and retrospective motion correction at 3T. by Corbin N, Trotier AJ, Anandra S, Kadalie E, Dallet L, Miraux S, and Ribot EJ, Magn Reson Med.
Abstract
Purpose: Several barriers prevent the use of whole-brain T2 mapping in routine use despite increasing interest in this parameter. One of the main barriers is the long scan time resulting in patient discomfort and motion corrupted data. To address this challenge, a method for accurate whole-brain T2 mapping with a limited acquisition time and motion correction capabilities is investigated.
Methods: A 3D radial multi-echo spin-echo sequence was implemented with optimized sampling trajectory enabling the estimation of intra-scan motion, subsequently used to correct the raw data. Motion corrected echo images are then reconstructed with linear subspace constrained reconstruction. Experiments were carried out on phantom and volunteers at 3T to evaluate the accuracy of the T2 estimation, the sensitivity to lesions and the efficiency of the correction on motion corrupted data.
Results: Whole-brain T2 mapping acquired in less than 7 min enabled the depiction of lesions in the white matter with longer T2. Data retrospectively corrupted with typical motion traces of pediatric patients highly benefited from the motion correction by reducing the error in T2 estimates within the lesions. All datasets acquired on seven volunteers, with deliberate motion, also showed that motion corrupted T2 maps could be improved with the retrospective motion correction both at the voxel level and the structure level.
Conclusion: A whole-brain T2 mapping sequence with retrospective intra-scan motion correction and reasonable acquisition time is proposed. The method necessitates advanced iterative reconstruction strategies but no additional navigator, external device, or increased scan time is required.
Keywords: T2 mapping; motion correction; radial sampling.