References of "Bettendorff, Lucien"
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See detailThiamine derivatives in excitable tissues: Metabolism, deficiency and neurodegenerative diseases
Bettendorff, Lucien ULiege; Wins, Pierre

in Pandalai, S. G. (Ed.) Recent Research Developments in Neurochemistry, vol 2, part 1 (1999)

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See detailThe molecular neuron-glia couple and epileptogenesis
Grisar, Thierry ULiege; Lakaye, Bernard ULiege; Thomas, Elizabeth et al

in Delgado-Escueta, A. V.; Wilson, W. A.; Olsen, R. W. (Eds.) et al Jasper's Basic Mechanisms of the Epilepsies, 3rd edition (1999)

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See detailReversibility of thiamine deficiency-induced partial necrosis and mitochondrial uncoupling by addition of thiamine to neuroblastoma cell suspensions.
Bettendorff, Lucien ULiege; Goessens, Guy ULiege; Sluse, Francis ULiege

in Molecular and Cellular Biochemistry (1997), 174(1-2), 121-4

Culture of neuroblastoma cells in the presence of low thiamine concentration (16 nM) and of the transport inhibitor amprolium leads to the appearance of signs of necrosis: the chromatin condenses, the ... [more ▼]

Culture of neuroblastoma cells in the presence of low thiamine concentration (16 nM) and of the transport inhibitor amprolium leads to the appearance of signs of necrosis: the chromatin condenses, the oxygen consumption decreases and is uncoupled, the mitochondrial cristae are disorganized, the thiamine diphosphate-dependent dehydrogenase activities are impaired. When 10 microM thiamine are added to these cells, the basal respiration increases, the coupled respiration is restored and mitochondrial morphology is recovered within 1 h. Addition of succinate, which is oxidized via a thiamine diphosphate-independent dehydrogenase, to digitonin-permeabilized cells immediately restores a coupled respiration. Our results suggest that the slowing of the citric acid cycle is the cause of the biochemical lesion induced by severe thiamine deficiency and that part of the mitochondria remain functional. [less ▲]

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See detailLow Thiamine Diphosphate Levels in Brains of Patients with Frontal Lobe Degeneration of the Non-Alzheimer's Type
Bettendorff, Lucien ULiege; Mastrogiacomo, Frank; Wins, Pierre et al

in Journal of Neurochemistry (1997), 69(5), 2005-2010

We compared the thiamine and thiamine phosphate contents in the frontal, temporal, parietal, and occipital cortex of six patients with frontal lobe degeneration of the non-Alzheimer's type (FNAD) or ... [more ▼]

We compared the thiamine and thiamine phosphate contents in the frontal, temporal, parietal, and occipital cortex of six patients with frontal lobe degeneration of the non-Alzheimer's type (FNAD) or frontotemporal dementia with five age-, postmortem delay-, and agonal status-matched control subjects. Our results reveal a 40-50% decrease in thiamine diphosphate (TDP) in the cortex of FNAD patients, whereas thiamine monophosphate was increased 49-119%. TDP synthesizing and hydrolyzing enzymes were unaffected. The activity of citrate synthase, a mitochondrial marker enzyme, was decreased in the frontal cortex of patients with FNAD, but no correlation with TDP content was found. These results suggest that decreased contents of TDP, which is essentially mitochondrial, is a specific feature of FNAD. As TDP is an essential cofactor for oxidative metabolism and neurotransmitter synthesis, and because low thiamine status (compared with other species) is a constant feature in humans, a nearly 50% decrease in cortical TDP content may contribute significantly to the clinical symptoms observed in FNAD. This study also provides a basis for a trial of thiamine, to improve the cognitive status of the patients. [less ▲]

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See detailParadoxical Sleep Deprivation Increases the Content of Glutamate and Glutamine in Rat Cerebral Cortex
Bettendorff, Lucien ULiege; Sallanon-Moulin, M.; Touret, Monique et al

in Sleep (1996), 19(1), 65-71

We investigated the influence of the sleep/waking cycle, the effects of paradoxical sleep deprivation (PSD) and of the vigilance-promoting drug modafinil on the amino acid contents of rat brain cortex. No ... [more ▼]

We investigated the influence of the sleep/waking cycle, the effects of paradoxical sleep deprivation (PSD) and of the vigilance-promoting drug modafinil on the amino acid contents of rat brain cortex. No significant nycthemeral variations in amino acid levels could be detected. PSD (12-24 hours), using the water tank method, significantly increased the levels of glutamate and glutamine. The increase was still observed after the sleep rebound period. gamma-Aminobutyric acid (GABA) levels did not change significantly during the instrumental sleep deprivation but increased during the rebound period. Control experiments indicate that the increase in glutamate and glutamine levels is due to PSD rather than to the stress associated with the experimental procedure. The increase in glutamate content cannot arise only from transamination reactions, because the levels of other amino acids (such as aspartate) did not decrease. Modafinil treatment did not significantly modify the brain cortex content of any of the amino acids tested. [less ▲]

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See detailBrain Levels of Thiamine and Its Phosphate Esters in Friedreich's Ataxia and Spinocerebellar Ataxia Type 1
Bettendorff, Lucien ULiege; Mastrogiacomo, Frank; LaMarche, J. et al

in Movement Disorders : Official Journal of the Movement Disorder Society (1996), 11(4), 437-439

Decreased blood and cerebrospinal fluid levels of thiamine have been reported in patients with spinocerebellar ataxia disorders. To determine whether a thiamine deficiency is present in the brain, we ... [more ▼]

Decreased blood and cerebrospinal fluid levels of thiamine have been reported in patients with spinocerebellar ataxia disorders. To determine whether a thiamine deficiency is present in the brain, we measured levels of thiamine and its phosphate esters thiamine monophosphate (TMP) and thiamine diphosphate (TDP), in postmortem cerebellar and cerebral cortices of patients with Friedreich's ataxia (FA) and spinocerebellar ataxia type 1 (SCA1). Brain levels of free (nonphosphorylated) thiamine, TMP, TDP, and total thiamine in FA and SCA1 were, on average, not significantly different from control values. However, a nonsignificant trend was observed for slightly reduced levels of TDP and total thiamine in cerebellar cortex of the SCA1 patients, a finding that might be related to the severe neuronal damage in this brain area. We conclude that in FA, brain thiamine concentrations are normal, whereas in SCA1 the levels are, at most, only slightly reduced. [less ▲]

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See detailImmunoreactive levels of α-ketoglutarate dehydrogenase subunits in Friedreich's ataxia and spinocerebellar ataxia type 1
Mastrogiacomo, Frank; LaMarche, Jacques; Dozic, Slobodan et al

in Neurodegeneration : A Journal for Neurodegenerative Disorders, Neuroprotection, and Neuroregeneration (1996), 5

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See detailA Non-Cofactor Role of Thiamine Derivatives in Excitable Cells?
Bettendorff, Lucien ULiege

in Archives of Physiology & Biochemistry (1996), 104(6), 745-751

Thiamine diphosphate (TDP) is an important cofactor of pyruvate (PDH) and alpha-ketoglutarate (KGDH) dehydrogenases and transketolase. Thiamine deficiency leads to reversible and irreversible brain ... [more ▼]

Thiamine diphosphate (TDP) is an important cofactor of pyruvate (PDH) and alpha-ketoglutarate (KGDH) dehydrogenases and transketolase. Thiamine deficiency leads to reversible and irreversible brain lesions due to impaired oxidative metabolism. A specific non-cofactor role for thiamine has also been proposed in excitable cells and thiamine triphosphate (TTP) might be involved in the regulation of ion channels. Thiamine is taken up by neuroblastoma cells through a high affinity transporter. Inside the cells, it is rapidly phosphorylated to TDP. This high turnover TDP pool is the precursor for TTP. Most of the TDP however has a low turnover and is associated with PDH and KGDH in mitochondria. In excised inside-out patches from neuroblastoma cells, TTP, at a concentration of 1 microM, activates chloride channels of large unitary conductance, the so-called maxi-Cl- channels. These channels are inhibited by oxythiamine from the outide. In addition to the role of TTP in the regulation of chloride channels, thiamine itself, or a presently unknown analog, may have trophic effects on neuronal cells. [less ▲]

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See detailThiamine, Thiamine Phosphates, and Their Metabolizing Enzymes in Human Brain
Bettendorff, Lucien ULiege; Mastrogiacomo, Frank; Kish, Stephen J et al

in Journal of Neurochemistry (1996), 66(1), 250-8

Total thiamine (the sum of thiamine and its phosphate esters) concentrations are two- to fourfold lower in human brain than in the brain of other mammals. There were no differences in the total thiamine ... [more ▼]

Total thiamine (the sum of thiamine and its phosphate esters) concentrations are two- to fourfold lower in human brain than in the brain of other mammals. There were no differences in the total thiamine content between biopsied and autopsied human brain, except that in the latter, thiamine triphosphate was undetectable. The main thiamine phosphate-metabolizing enzymes could be detected in autopsied brain, and the kinetic parameters were comparable to those reported in other species. Thiamine diphosphate levels were lowest in hippocampus (15 +/- 4 pmol/mg of protein) and highest in mammillary bodies (24 +/- 4 pmol/mg of protein). Maximal levels of thiamine and its phosphate ester were found to be present at birth. In parietal cortex and globus pallidus, mean levels of total thiamine in the oldest age group (77-103 years) were, respectively, 21 and 26% lower than those in the middle age group (40-55 years). Unlike cerebral cortex, the globus pallidus showed a sharp drop in thiamine diphosphate levels during infancy, with concentrations in the oldest group being only approximately 50% of the levels present during the first 4 months of life. These data, consistent with previous observations conducted in blood, suggest a tendency toward decreased thiamine status in older people. [less ▲]

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See detailBrain protein and alpha-ketoglutarate dehydrogenase complex activity in Alzheimer's disease
Mastrogiacomo, Frank; Lindsay, J. Gordon; Bettendorff, Lucien ULiege et al

in Annals of Neurology (1996), 39

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See detailBrain thiamine, its phosphate esters, and its metabolizing enzymes in Alzheimer's disease.
Mastrogiacomo, Frank; Bettendorff, Lucien ULiege; Grisar, Thierry ULiege et al

in Annals of Neurology (1996), 39

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See detailThiamine Deficiency--Induced Partial Necrosis and Mitochondrial Uncoupling in Neuroblastoma Cells Are Rapidly Reversed by Addition of Thiamine
Bettendorff, Lucien ULiege; Sluse, Francis ULiege; Goessens, Guy ULiege et al

in Journal of Neurochemistry (1995), 65(5), 2178-2184

Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the ... [more ▼]

Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the chromatin condenses in dark patches, the oxygen consumption decreases, mitochondria are uncoupled, and their cristae are disorganized. Glutamate formed from glutamine is no longer oxidized and accumulates, suggesting that the thiamine diphosphate-dependent alpha-ketoglutarate dehydrogenase activity is impaired. When thiamine (10 microM) is added to the cells, the O2 consumption increases, respiratory control is restored, and normal cell and mitochondrial morphology is recovered within 1 h. Succinate, which is oxidized via the thiamine diphosphate-independent succinate dehydrogenase, is also able to restore a normal O2 consumption (with respiratory control) in digitonin-permeabilized thiamine-deficient cells. Our results therefore suggest that the slowing of the citric acid cycle is the main cause of the biochemical lesion induced by thiamine deficiency as observed in Wernicke's encephalopathy. [less ▲]

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See detailThiamine Deficiency in Cultured Neuroblastoma Cells: Effect on Mitochondrial Function and Peripheral Benzodiazepine Receptors
Bettendorff, Lucien ULiege; Goessens, Guy ULiege; Sluse, Francis ULiege et al

in Journal of Neurochemistry (1995), 64(5), 2013-2021

When neuroblastoma cells were transferred to a medium of low (6 nM) thiamine concentration, a 16-fold decrease in total intracellular thiamine content occurred within 8 days. Respiration and ATP levels ... [more ▼]

When neuroblastoma cells were transferred to a medium of low (6 nM) thiamine concentration, a 16-fold decrease in total intracellular thiamine content occurred within 8 days. Respiration and ATP levels were only slightly affected, but addition of a thiamine transport inhibitor (amprolium) decreased ATP content and increased lactate production. Oxygen consumption became low and insensitive to oligomycin and uncouplers. At least 25% of mitochondria were swollen and electron translucent. Cell mortality increased to 75% within 5 days. [3H]PK 11195, a specific ligand of peripheral benzodiazepine receptors (located in the outer mitochondrial membrane) binds to the cells with high affinity (KD = 1.4 +/- 0.2 nM). Thiamine deficiency leads to an increase in both Bmax and KD. Changes in binding parameters for peripheral benzodiazepine receptors may be related to structural or permeability changes in mitochondrial outer membranes. In addition to the high-affinity (nanomolar range) binding site for peripheral benzodiazepine ligands, there is a low-affinity (micromolar range) saturable binding for PK 11195. At micromolar concentrations, peripheral benzodiazepines inhibit thiamine uptake by the cells. Altogether, our results suggest that impairment of oxidative metabolism, followed by mitochondrial swelling and disorganization of cristae, is the main cause of cell mortality in severely thiamine-deficient neuroblastoma cells. [less ▲]

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See detailThiamine Homeostasis in Neuroblastoma Cells
Bettendorff, Lucien ULiege

in Neurochemistry International (1995), 26(3), 295-302

We recently showed that thiamine uptake by neuroblastoma cells is mediated by two saturable transport system: the first with high affinity for thiamine (Km = 35 nM) is blocked by veratridine; the other ... [more ▼]

We recently showed that thiamine uptake by neuroblastoma cells is mediated by two saturable transport system: the first with high affinity for thiamine (Km = 35 nM) is blocked by veratridine; the other, with low affinity is blocked by Ca2+. The driving force for thiamine uptake is its phosphorylation to thiamine diphosphate (TDP) by thiamine pyrophosphokinase and subsequent binding of this cofactor to apoenzymes. Our results suggest that cells of neuronal origin possess mechanisms regulating the intracellular concentration of thiamine. At low external thiamine, the vitamin is taken up by a high-affinity transporter and pyrophosphorylated in thiamine diphosphate (TDP): this is the TDP pool of slow turnover. An intraover extracellular concentration gradient of free thiamine is observed at low external concentration of the vitamin. At higher external thiamine concentration, TDP accumulation is limited by the binding capacity to the apoenzymes and unbound TDP (i.e. a small pool of fast turnover) is quickly hydrolyzed. Thiamine is slowly released by the cells by at least two different mechanisms. The first, accounting for a maximum of 50% of total thiamine release, is stimulated by external thiamine and is blocked by veratridine, suggesting that it is a self-exchange mechanism catalyzed by the high affinity thiamine transporter. The remaining thiamine efflux is neither sensitive to veratridine nor to Ca2+ and its mechanism is unknown. About 25% of intracellular thiamine is not released, even after treatment of the cells with digitonin, thus maintaining an apparent gradient. This suggests a binding or sequestration in intracellular compartments.(ABSTRACT TRUNCATED AT 250 WORDS) [less ▲]

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See detailAn Atypical Anion Transporter Functioning at Acid pH in Neuroblastoma Cells
Bettendorff, Lucien ULiege; Margineanu, Ilca; Wins, Pierre et al

in Biochemical and Biophysical Research Communications (1995), 207(1), 375-381

At pH 7.4, 36Cl- uptake by neuroblastoma cells was Na(+)-independent, saturable and blocked by submicromolar concentrations of DIDS. This suggests that at this pH, Cl- transport is mediated by an ... [more ▼]

At pH 7.4, 36Cl- uptake by neuroblastoma cells was Na(+)-independent, saturable and blocked by submicromolar concentrations of DIDS. This suggests that at this pH, Cl- transport is mediated by an exchanger analogous to erythroid band 3. At pH 6. [less ▲]

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See detailTransport and metabolism of thiamine
Bettendorff, Lucien ULiege

Scientific conference (1994)

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See detailThiamine in Excitable Tissues: Reflections on a Non-Cofactor Role
Bettendorff, Lucien ULiege

in Metabolic Brain Disease (1994), 9(3), 183-209

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