Pyritinol has been used clinically in a wide range of disorders including cerebral circulatory disorders, alcoholism, dyslexia, behavioral disorders in children, and stroke.
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Pyritinol has been used following head injury and cerebral trauma. Pyritinol has reduced the normal high death rate in such cases and has rapidly returned coma patients to more or less normal waking consciousness, even when the brain injuries were so severe the patient ultimately died. Pyritinol has the ability to enhance glucose transport through the blood-brain barrier. Although the brain is usually less than 2% of total bodyweight, the brain uses about 20% of the body’s total energy production. Under normal, non-fasting conditions, the brain can only ‘burn’ glucose (sugar) for fuel. Unlike virtually all other body cells, nerve cells cannot use fat as an energy fuel. Brain cells also cannot store any significant amount of glucose – they are completely dependent upon a continuous delivery of glucose from the blood, through the blood-brain barrier. Thus, brain glucose uptake is a major rate-limiting factor for crucial brain energy production. Pyritinol has the ability to increase glucose transport through the blood-brain barrier.
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|REFERENCESK. Kitamura (1981) “Therapeutic Effect of Pyritinol on Sequelae of Head Injuries” J Int Med Res 9, 215-21.
G. Dalle Ore et al (1980) “The Influence of the Administration of Pyritinol on the Clinical Course of Traumatic Coma”, J Neuroserg Sci 24, 1-8.
E.M. Lemmel (1993) “Comparison of Pyritinol and Auranofin in the Treatment of Rheumatoid Arthritis” Br J Rheumatol 32, 375-82.
I. Hindmarch et al (1990) “Psychpharmacalogical Effects of Pyritinol in Normal Volunteers” Neuropsychobiol 24, 159-64.
A. Pavlik & J. Pilar (1989) “Protection of Cell Proteins Against Free-Radical Attack by Nootropic Drugs: Scavenger Effects of Pyritinol Confirmed by Electron Spin Resonance Spectroscopy” Nueropharmacol 28, 557-61.
S. Hoyer et al (1977) “Effect of Pyritinol-HCL on Blood Flow and Oxidative Metabolism of the Brain in Patients with Dementia” Arzneim Forsch/Drug Res 27, 671-74.
J. Elferink & B. de Koster (1993) “Differential Stimulation of Neutrophil Functions by Pyritinol” Int J Immunopharmac 15, 641-46.
H.-R. Olpe et al (1985) “Locus Coeruleus as a Target for Psychogeriatric Agents” Ann NY Acad Sci 444, 394-405.
G. Logue et al (1974) “The Effects of Pyrithioxine on the Behavior and Intellectual Functioning of Learning-Disabled Children” S.Afr Med J 48, 2245-46.
D. Lane O’Kelly (1975) “Pyritinol in the Treatment of Chronic Alcoholics” J Int Med Res 3, 323-27.
K. Fischhof et al (1992) “Therapeutic Efficacy of Pyritinol in Patients with Senile Dementia of the Alzheimer Type (SDAT) and Multi-Infarct Dementia (MID)” Neuropsychobiol 26, 65-70.
A. Cooper & R. Magnus (1980) “A Placebo-Controlled Study of Pyritinol in Dementia” Pharmatherapeutica 2, 317-22. R. Branconnier (1983) “The Efficacy of the Cerebral Metabolic Enhancers in the Treatment of Senile Dementia” Psychopharmacol Bull 1983 Spring;19(2):212-9.