pyruvic acid has been researched along with Seizures in 24 studies
Pyruvic Acid: An intermediate compound in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is retarded and it accumulates in the tissues, especially in nervous structures. (From Stedman, 26th ed)
pyruvic acid : A 2-oxo monocarboxylic acid that is the 2-keto derivative of propionic acid. It is a metabolite obtained during glycolysis.
Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or seizure disorder.
| Excerpt | Relevance | Reference |
|---|---|---|
| "It has been postulated that triheptanoin can ameliorate seizures by supplying the tricarboxylic acid cycle with both acetyl-CoA for energy production and propionyl-CoA to replenish cycle intermediates." | 3.79 | Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain. ( Good, LB; Ma, Q; Malloy, CR; Marin-Valencia, I; Pascual, JM, 2013) |
| "In females with a pyruvate dehydrogenase deficiency E1alpha owing to the mutation in the subunit E1alpha of the pyruvate dehydrogenase complex West's syndrome associated with large ventricles and corpus callosum agenesis on magnetic resonance imaging can be the main feature of the disease." | 2.41 | Defects of pyruvate metabolism and the Krebs cycle. ( De Meirleir, L, 2002) |
| "Dichloroacetic acid (DCA) has been shown to prevent cell death." | 1.72 | Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure. ( Choi, BY; Choi, HC; Hong, DK; Kang, BS; Kho, AR; Lee, SH; Park, MK; Song, HK; Suh, SW, 2022) |
| "Early post-traumatic seizures are one potential mechanism for metabolic crisis and hence could be a therapeutic target." | 1.43 | Metabolic crisis occurs with seizures and periodic discharges after brain trauma. ( Buitrago-Blanco, M; Claassen, J; McArthur, D; Nuwer, M; Prins, M; Tu, B; Tubi, M; Velazquez, AG; Vespa, P, 2016) |
| "Hypoxia and seizures early in life can cause multiple neurological deficits and even chronic epilepsy." | 1.37 | Perinatal hypoxia induces a long-lasting increase in unstimulated gaba release in rat brain cortex and hippocampus. The protective effect of pyruvate. ( Himmelreich, N; Parkhomenko, N; Pozdnyakova, N; Yatsenko, L, 2011) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 8 (33.33) | 18.7374 |
| 1990's | 2 (8.33) | 18.2507 |
| 2000's | 4 (16.67) | 29.6817 |
| 2010's | 7 (29.17) | 24.3611 |
| 2020's | 3 (12.50) | 2.80 |
| Authors | Studies |
|---|---|
| De La Rossa, A | 1 |
| Laporte, MH | 1 |
| Astori, S | 1 |
| Marissal, T | 1 |
| Montessuit, S | 1 |
| Sheshadri, P | 1 |
| Ramos-Fernández, E | 1 |
| Mendez, P | 1 |
| Khani, A | 1 |
| Quairiaux, C | 1 |
| Taylor, EB | 1 |
| Rutter, J | 1 |
| Nunes, JM | 1 |
| Carleton, A | 1 |
| Duchen, MR | 1 |
| Sandi, C | 1 |
| Martinou, JC | 1 |
| Bharathi, SS | 1 |
| Zhang, BB | 1 |
| Paul, E | 1 |
| Zhang, Y | 1 |
| Schmidt, AV | 1 |
| Fowler, B | 1 |
| Wu, Y | 1 |
| Tiemeyer, M | 1 |
| Inamori, KI | 1 |
| Inokuchi, JI | 1 |
| Goetzman, ES | 1 |
| Lee, SH | 6 |
| Choi, BY | 3 |
| Kho, AR | 3 |
| Hong, DK | 3 |
| Kang, BS | 3 |
| Park, MK | 3 |
| Choi, HC | 3 |
| Song, HK | 3 |
| Suh, SW | 3 |
| Ching, CK | 1 |
| Mak, CM | 1 |
| Au, KM | 1 |
| Chan, KY | 1 |
| Yuen, YP | 1 |
| Yau, EK | 1 |
| Ma, LC | 1 |
| Chow, HL | 1 |
| Chan, AY | 1 |
| Simeone, KA | 1 |
| Matthews, SA | 1 |
| Samson, KK | 1 |
| Simeone, TA | 1 |
| Vespa, P | 1 |
| Tubi, M | 1 |
| Claassen, J | 1 |
| Buitrago-Blanco, M | 1 |
| McArthur, D | 1 |
| Velazquez, AG | 1 |
| Tu, B | 1 |
| Prins, M | 1 |
| Nuwer, M | 1 |
| Pozdnyakova, N | 1 |
| Yatsenko, L | 1 |
| Parkhomenko, N | 1 |
| Himmelreich, N | 1 |
| GOUNELLE, H | 1 |
| RAOUL, Y | 1 |
| Rossignol, DA | 1 |
| Frye, RE | 1 |
| Kovac, S | 1 |
| Abramov, AY | 1 |
| Walker, MC | 1 |
| Marin-Valencia, I | 1 |
| Good, LB | 1 |
| Ma, Q | 1 |
| Malloy, CR | 1 |
| Pascual, JM | 1 |
| De Meirleir, L | 1 |
| LODDING, C | 1 |
| BARRETO, RC | 1 |
| MANO, DB | 1 |
| ISRAELS, S | 1 |
| HAWORTH, JC | 1 |
| GOURLEY, B | 1 |
| FORD, JD | 1 |
| Barnérias, C | 1 |
| Giurgea, I | 1 |
| Hertz-Pannier, L | 1 |
| Bahi-Buisson, N | 1 |
| Boddaert, N | 1 |
| Rustin, P | 1 |
| Rotig, A | 1 |
| Desguerre, I | 1 |
| Munnich, A | 1 |
| de Lonlay, P | 1 |
| Gasior, M | 1 |
| French, A | 1 |
| Joy, MT | 1 |
| Tang, RS | 1 |
| Hartman, AL | 1 |
| Rogawski, MA | 1 |
| BAIN, JA | 1 |
| POLLOCK, GH | 1 |
| Höller, M | 1 |
| Breuer, H | 1 |
| Fleischhauer, K | 1 |
| Siesjö, BK | 1 |
| Schürmann, M | 1 |
| Engelbrecht, V | 1 |
| Lohmeier, K | 1 |
| Lenard, HG | 1 |
| Wendel, U | 1 |
| Gärtner, J | 1 |
| Thoresen, M | 1 |
| Hallström, A | 1 |
| Whitelaw, A | 1 |
| Puka-Sundvall, M | 1 |
| Løberg, EM | 1 |
| Satas, S | 1 |
| Ungerstedt, U | 1 |
| Steen, PA | 1 |
| Hagberg, H | 1 |
| Ido, Y | 1 |
| Chang, K | 1 |
| Woolsey, TA | 1 |
| Williamson, JR | 1 |
| Haas, RH | 1 |
| Rice, MA | 1 |
| Trauner, DA | 1 |
| Merritt, TA | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Exogenous Sodium Lactate Infusion in Traumatic Brain Injury (ELI-TBI)[NCT02776488] | Phase 2 | 0 participants (Actual) | Interventional | 2020-09-30 | Withdrawn (stopped due to The manufacturer of sodium lactate has stopped making the medication) | ||
| Post Study Continuation of C7 for G1D[NCT02018302] | 0 participants | Expanded Access | No longer available | ||||
| Treatment Development of Triheptanoin for Glucose Transporter Type I Deficiency[NCT02021526] | Phase 1/Phase 2 | 0 participants (Actual) | Interventional | 2015-12-31 | Withdrawn (stopped due to NIH funding resulted in new clinical trial) | ||
| The Glucose Transporter Type I Deficiency (G1D) Registry[NCT02013583] | 750 participants (Anticipated) | Observational [Patient Registry] | 2013-12-31 | Recruiting | |||
| Treatment Development of Triheptanoin (C7) for Glucose Transporter Type I Deficiency (G1D): A Phase I Maximum Tolerable Dose Trial[NCT03041363] | Phase 1 | 12 participants (Actual) | Interventional | 2017-03-29 | Completed | ||
| Clinical Trial of Citric Acid Cycle Stimulation in Energy-deficiency States: Treatment Development for Glucose Transporter Type I Deficiency Syndrome (G1D) (NMTUT 2010B)[NCT02018315] | Phase 1 | 14 participants (Actual) | Interventional | 2012-01-31 | Completed | ||
| An Open-Label Trial of Triheptanoin in Patients With Glucose Transporter Type-1 Deficiency Syndrome (GLUT1 DS)[NCT02036853] | Phase 2 | 20 participants (Actual) | Interventional | 2014-02-20 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Magnetic Resonance Imaging (MRI) used to calculate brain metabolic rate. Brain metabolic rate compared before oil ingestion (Baseline), 90 minutes after oil ingestion, and after 3 months of daily oil ingestion in each participant. Triheptanoin metabolism may lead to increased oxygen consumption only while the brain undergoes a reduction of ictogenesis. We hypothesize that when ictogenesis is abolished by triheptanoin or absent at baseline, triheptanoin exerts little or no effect on CMR02. (NCT02018315)
Timeframe: 3 months
| Intervention | Participants (Count of Participants) |
|---|---|
| Experimental: Triheptanoin | 5 |
Visual analysis of EEG recording to determine the fraction of spike-range within the area of recording. (NCT02018315)
Timeframe: 1 day
| Intervention | Participants (Count of Participants) |
|---|---|
| Experimental: Triheptanoin | 13 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. The table below represents the change in seizure frequency from baseline for each time point. (NCT02036853)
Timeframe: Baseline and four yrs
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | -8.3 |
| Schedule B | -80.3 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. The table below represents the change in seizure frequency from baseline for each time point. (NCT02036853)
Timeframe: Baseline and five yrs
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | 23 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. The table below represents the change in seizure frequency from baseline for each time point. (NCT02036853)
Timeframe: Baseline and one yr
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | -6.5 |
| Schedule B | -110.5 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. (NCT02036853)
Timeframe: Baseline and 13 weeks
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | 4.4 |
| Schedule B | 189.5 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. The table below represents the change in seizure frequency from baseline for each time point. (NCT02036853)
Timeframe: Baseline and 18 months
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | -5.8 |
| Schedule B | -112.7 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. The table below represents the change in seizure frequency from baseline for each time point. (NCT02036853)
Timeframe: Baseline and two yrs
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | -6 |
| Schedule B | -61.25 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. The table below represents the change in seizure frequency from baseline for each time point. (NCT02036853)
Timeframe: Baseline and 26 weeks
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | -5.6 |
| Schedule B | -78 |
A seizure diary was used to track date, type, number, and unusual presentation of seizures. Subjects were given a seizure diary at screening to record daily seizure activity for incremental periods of time. Unless otherwise waived, subjects complete this form daily during the screening period and for two weeks prior to each subsequent study visit. The table below represents the change in seizure frequency from baseline for each time point. (NCT02036853)
Timeframe: Baseline and three yrs
| Intervention | seizures/two weeks (Mean) |
|---|---|
| Schedule A | -0.8 |
| Schedule B | -77 |
4 reviews available for pyruvic acid and Seizures
| Article | Year |
|---|---|
Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis.
Topics: Adenosine Triphosphate; Adolescent; Animals; Biomarkers; Brain; Child; Child Development Disorders, | 2012 |
Energy depletion in seizures: anaplerosis as a strategy for future therapies.
Topics: Adenosine Triphosphate; Animals; Citric Acid Cycle; Diet, Ketogenic; Energy Metabolism; Humans; Neur | 2013 |
Defects of pyruvate metabolism and the Krebs cycle.
Topics: Brain; Citric Acid Cycle; Diagnosis, Differential; Fumarate Hydratase; Humans; Magnetic Resonance Im | 2002 |
Lactic acidosis in the brain: occurrence, triggering mechanisms and pathophysiological importance.
Topics: Acidosis; Animals; Blood Glucose; Brain; Brain Ischemia; Carbon Dioxide; Glucose; Hypoxia, Brain; In | 1982 |
20 other studies available for pyruvic acid and Seizures
| Article | Year |
|---|---|
Paradoxical neuronal hyperexcitability in a mouse model of mitochondrial pyruvate import deficiency.
Topics: 3-Hydroxybutyric Acid; Animals; Anion Transport Proteins; Biological Transport; Calcium; Gene Expres | 2022 |
GM3 synthase deficiency increases brain glucose metabolism in mice.
Topics: Animals; Brain; G(M3) Ganglioside; Glucose; Mice; Mice, Knockout; Pyruvic Acid; Seizures; Sialyltran | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
Combined Treatment of Dichloroacetic Acid and Pyruvate Increased Neuronal Survival after Seizure.
Topics: Adenosine Triphosphate; Animals; Dichloroacetic Acid; Glucose; Pyruvate Dehydrogenase Complex; Pyruv | 2022 |
A patient with congenital hyperlactataemia and Leigh syndrome: an uncommon mitochondrial variant.
Topics: Acidosis, Lactic; DNA, Mitochondrial; Female; Humans; Infant; Lactic Acid; Leigh Disease; Pyruvic Ac | 2013 |
Targeting deficiencies in mitochondrial respiratory complex I and functional uncoupling exerts anti-seizure effects in a genetic model of temporal lobe epilepsy and in a model of acute temporal lobe seizures.
Topics: Adenosine Triphosphate; alpha-Tocopherol; Animals; Ascorbic Acid; Disease Models, Animal; Electric S | 2014 |
Metabolic crisis occurs with seizures and periodic discharges after brain trauma.
Topics: Adult; Aged; Aged, 80 and over; Brain Injuries; Electroencephalography; Female; Humans; Lactic Acid; | 2016 |
Perinatal hypoxia induces a long-lasting increase in unstimulated gaba release in rat brain cortex and hippocampus. The protective effect of pyruvate.
Topics: Animals; Animals, Newborn; Cerebral Cortex; Dose-Response Relationship, Drug; Extracellular Space; g | 2011 |
Increase in the level of pyruvic acid in the blood after convulsive therapy by electro-shock.
Topics: Blood; Pyruvic Acid; Seizures; Therapeutics | 1945 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Heptanoate as a neural fuel: energetic and neurotransmitter precursors in normal and glucose transporter I-deficient (G1D) brain.
Topics: Acetyl Coenzyme A; Animals; Anticonvulsants; Brain; Brain Chemistry; Energy Metabolism; Glucose; Glu | 2013 |
Investigations into the pyruvic acid concentration in blood from children with convulsive fits and petit mal and an assessment of the significance of muscular activity on pyruvic acid estimations in infants in general.
Topics: Child; Epilepsy, Absence; Humans; Infant; Pyruvates; Pyruvic Acid; Seizures | 1952 |
Prevention of the convulsivant and lethal effects of isonicotinic acid hydrazide by pyruvic acid.
Topics: Biomedical Research; Convulsants; Isoniazid; Pyruvates; Pyruvic Acid; Seizures | 1961 |
CHRONIC ACIDOSIS DUE TO AN ERROR IN LACTATE AND PYRUVATE METABOLISM. REPORT OF TWO CASES.
Topics: Acetoacetates; Acidosis; Blood; Blood Gas Analysis; Carbohydrate Metabolism; Carbohydrate Metabolism | 1964 |
Respiratory chain deficiency in a female with Aicardi-Goutières syndrome.
Topics: Basal Ganglia; Calcinosis; Chromatography, Gas; Dementia, Vascular; Female; Humans; Interferon-alpha | 2006 |
The anticonvulsant activity of acetone, the major ketone body in the ketogenic diet, is not dependent on its metabolites acetol, 1,2-propanediol, methylglyoxal, or pyruvic acid.
Topics: Acetone; Animals; Anticonvulsants; Diet Therapy; Disease Models, Animal; Epilepsy; Ketone Bodies; Ma | 2007 |
Normal and seizure levels of lactate, pyruvate and acid-soluble phosphates in the cerebellum and cerebrum.
Topics: Brain Chemistry; Cerebellum; Cerebrum; Humans; Lactic Acid; Phosphates; Pyruvic Acid; Seizures; Tele | 1949 |
An improved method for perfusion of the isolated brain of the rat-influence of perfusion conditions and application of analeptic and anticonvulsant drugs.
Topics: Adenosine Triphosphate; Animals; Anticonvulsants; Brain; Central Nervous System Stimulants; Lactates | 1983 |
Cerebral metabolic changes in biotinidase deficiency.
Topics: Amidohydrolases; Biotin; Biotinidase; Brain; Electroencephalography; Humans; Infant; Lactic Acid; Ma | 1997 |
Lactate and pyruvate changes in the cerebral gray and white matter during posthypoxic seizures in newborn pigs.
Topics: Animals; Animals, Newborn; Cerebellum; Electroencephalography; Hypoxia; Lactic Acid; Microdialysis; | 1998 |
NADH: sensor of blood flow need in brain, muscle, and other tissues.
Topics: Animals; Brain; Cytosol; Lactic Acid; Muscle Contraction; Muscles; NAD; Physical Conditioning, Anima | 2001 |
Therapeutic effects of a ketogenic diet in Rett syndrome.
Topics: Ammonia; Blood Glucose; Child; Child, Preschool; Dietary Fats; Electroencephalography; Energy Intake | 1986 |