I just found this study, and thought it might be of interest. Interestingly, I also found an article, which I have put below this one, regarding d-lactic inhibiting astrocytes. There is a study underway in Australia, taking KDM's research further, regarding CFS and d-lactic, if anyone wants details, please let me know and I will send some links. Glynis A brain MRI study of chronic fatigue syndrome: Evidence of brainstem dysfunction and altered homeostasis Authors: Leighton R. Barnden, Benjamin Crouch, Richard Kwiatek, Richard Burnet, Anacleto Mernone, Steve Chryssidis, Garry Scroop, Peter Del Fante Publication: NMR in Biomedicine Abstract [accepted, pre-proof] To explore brain involvement in chronic fatigue syndrome (CFS), we have extended statistical parametric mapping of brain magnetic resonance (MR) images to whole-brain voxel-based regressions against clinical scores. Using SPM5 we performed voxel-based morphometry (VBM) and analysed T1- and T2-weighted spin-echo MR signal levels in 25 CFS subjects and 25 normal controls (NC). Clinical scores included CFS fatigue duration, a score based on the 10 most common CFS symptoms, the Bell score, HADS anxiety and depression, and hemodynamic parameters from 24 hour blood pressure monitoring. We also performed group hemodynamic score interaction regressions to detect locations where MR regressions were opposite for CFS and NC, thereby indicating abnormality in the CFS group. In the midbrain, white matter volume was observed to decrease with increasing fatigue duration. For T1-weighted MR and white matter volume, group hemodynamic score interactions were detected in the brainstem (strongest in midbrain grey matter), deep prefrontal white matter, the caudal basal pons and hypothalamus. A strong correlation in CFS between brainstem grey matter volume and pulse pressure suggested impaired cerebrovascular autoregulation. We argue that at least some of these changes could arise from astrocyte dysfunction. These results are consistent with an insult to the midbrain at fatigue onset that affects multiple feedback control loops to suppress cerebral motor and cognitive activity and disrupt local CNS homeostasis, including resetting of some elements of the autonomic nervous system. Inhibition of astrocytic energy metabolism by D-lactate exposure impairs memory. Gibbs ME, Hertz L. Department of Anatomy and Developmental Biology, Monash University, Clayton 3800, Australia. Abstract Bead discrimination learning in day-old chicken was inhibited by bilateral injection into the intermediate medial mesopallium (IMM), a homolog of the mammalian brain cortex, of the poorly metabolized enantiomer of L-lactate, D-lactate. The window of vulnerability extended from 10 min before training to 20 min after training. Unilateral injection 10 min before training inhibited only in the left IMM, whereas 10 min after training injection was only inhibitory if made into the right hemisphere. The pre-training administration caused memory loss from the earliest time tested whereas memory was maintained for another 20 min when D-lactate was injected 10 min post-training. The ability of acetate, an astrocyte-specific substrate, injected into the IMM to counteract the inhibitory effect was tested. Following D-lactate injection 10 min before training, rescue of memory immediately after training was achieved by acetate as long as aspartate, an oxaloacetate precursor, was also present. This suggests that pyruvate carboxylation is necessary for net synthesis of glutamate, which is known to occur at this time [Gibbs, M.E., Lloyd, H.G.E., Santa, T., Hertz, L., 2007. Glycogen is a preferred glutamate precursor during learning in 1-day-old chick: biochemical and behavioral evidence. J. Neurosci. Res., 85, 3326-3333]. However, acetate alone rescued memory 20 min post-training (following d-lactate injection 10 min after training), indicating that pyruvate at this time is used for energy production, consistent with memory inhibition by dinitrophenol. These findings suggest that D-lactate acts by inhibiting uptake of L-lactate into astrocytes (an extracellular effect) or metabolism of pyruvate in astrocytic mitochondria (an intracellular effect). An apparent lag phase between the administration of d-lactate and its inhibition of learning favors the latter possibility. Thus, under the present experimental conditions D-lactate acts as an astrocytic metabolic inhibitor rather than as an inhibitor of neuronal L-lactate uptake, as has occasionally been suggested. Analogously, a rare reversible neurological syndrome with memory deficits, D-lactate encephalopathy, may mainly or exclusively be due to astrocytic malfunction.