The Experts below are selected from a list of 57 Experts worldwide ranked by ideXlab platform
Jong-soon Choi - One of the best experts on this subject based on the ideXlab platform.
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A Case of Severe Brain Atrophy Found in the Man in His Twenties Who Drinks Moderate Amount of Alcohol
2016Co-Authors: Jae-wook Yoo, Jong-soon ChoiAbstract:Brain atrophy is caused by the neuronal loss and reduction in Betz Cell numbers. Among the many causes of brain atrophy, alcohol related atrophy is largely accounted for by a reduction in white matter volume. And the degree of brain atrophy correlates with the rate and amount of alcohol consumed over a lifetime, and it is at least partially reversible with alcohol abstinence. Alcohol-related brain damage mechanism correlates with that ethanol selectively and potently inhibits the function of NMDA receptors. Chronic alcoholics often have a low intake of folate, hence a sustained hyperhomocystenemia can frequently be observed, then this cause a pathological increase in receptor activity and subsequent excitotoxic damage. Even the consumption of light and moderate doses of alcohol lead to shrinkage of the brain and to increases in white matter volume and decrease in grey matter volume. We report the case of severe brai
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A Case of Severe Brain Atrophy Found in the Man in His Twenties Who Drinks Moderate Amount of Alcohol
Korean Journal of Family Medicine, 2010Co-Authors: Jae-wook Yoo, Jong-soon ChoiAbstract:Brain atrophy is caused by the neuronal loss and reduction in Betz Cell numbers. Among the many causes of brain atrophy, alcohol related atrophy is largely accounted for by a reduction in white matter volume. And the degree of brain atrophy correlates with the rate and amount of alcohol consumed over a lifetime, and it is at least partially reversible with alcohol abstinence. Alcohol-related brain damage mechanism correlates with that ethanol selectively and potently inhibits the function of NMDA receptors. Chronic alcoholics often have a low intake of folate, hence a sustained hyperhomocystenemia can frequently be observed, then this cause a pathological increase in receptor activity and subsequent excitotoxic damage. Even the consumption of light and moderate doses of alcohol lead to shrinkage of the brain and to increases in white matter volume and decrease in grey matter volume. We report the case of severe brain atrophy incidentally found at medical check-up in a young man who has drunken alcohol too much for 10 years.
Peter S. Spencer - One of the best experts on this subject based on the ideXlab platform.
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Toxic models of upper motor neuron disease
Journal of the Neurological Sciences, 1996Co-Authors: Albert C. Ludolph, Peter S. SpencerAbstract:Abstract Although neurotoxic models for progressive degeneration of both the anterior horn Cell and the Betz Cell do not exist, (neuro)lathyrism and neurocassavism (konzo) are examples of self-limiting neurotoxic disorders that predominantly target the Betz Cell. Both disorders are caused by the continuous intake of neurotoxic plant products (Lathyrus sativus and Manihot esculenta, respectively) which result in a virtually identical clinical picture of spastic paraparesis. A neurotoxic excitatory amino acid and AMPA agonist (β-N-oxalylamino- l -alanine, BOAA) is held largely responsible for lathyrism. Epidemics of konzo are strongly associated with increased intake of the cyanide-liberating glycoside linamarin by protein-poor subjects. Whereas an animal model for neurocassavism does not exist, macaques fed Lathyrus sativus or BOAA develop central motor deficits with corticospinal tract involvement. Estimated dosages of Lathyrus sativus used to induce beginning lathyrism in well-nourished primates are 10–20 fold greater than those associated with irreversible human neurolathyrism. Major unexplained aspects of both diseases are the factors which allow the suspected toxins to target Betsz Cells (blood-brain barrier, receptor distribution, Cellular energy metabolism), the latency to onset in both diseases, and how two separate etiologic factors trigger clinically similar disorders.
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Toxic models of upper motor neuron disease.
Journal of the neurological sciences, 1996Co-Authors: Albert C. Ludolph, Peter S. SpencerAbstract:Although neurotoxic models for progressive degeneration of both the anterior horn Cell and the Betz Cell do not exist, (neuro)lathyrism and neurocassavism (konzo) are examples of self limiting neurotoxic disorders that predominantly target the Betz Cell. Both disorders are caused by the continuous intake of neurotoxic plant products (Lathyrus sativus and Manihot esculenta, respectively) which result in a virtually identical clinical picture of spastic paraparesis. A neurotoxic excitatory amino acid and AMPA agonist (beta-N-oxalylamino-1-alanine, BOAA) is held largely responsible for lathyrism. Epidemics of konzo are strongly associated with increased intake of the cyanide-liberating glycoside linamarin by protein-poor subjects. Whereas an animal model for neurocassavism does not exist, macaques fed Lathyrus sativus or BOAA develop central motor deficits with corticospinal tract involvement. Estimated dosages of Lathyrus sativus used to induce beginning lathyrism in well-nourished primates are 10-20 fold greater than those associated with irreversible human neurolathyrism. Major unexplained aspects of both diseases are the factors which allow the suspected toxins to target Betsz Cells (blood-brain barrier, receptor distribution, Cellular energy metabolism), the latency to onset in both diseases, and how two separate etiologic factors trigger clinically similar disorders.
Alan Peters - One of the best experts on this subject based on the ideXlab platform.
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Axon terminals on Betz Cell somata of area 4 in rhesus monkey throughout adulthood.
The Anatomical record, 1992Co-Authors: Johannes Tigges, James G. Herndon, Alan PetersAbstract:Previous work in our laboratory demonstrated an age-related decline in the size of Betz Cell somata in cortical area 4 of the adult rhesus monkey brain. The present study was conducted to determine whether changes might also occur in the axon terminals upon these cortical Cells. Tissue from area 4 was collected from seven rhesus monkeys and prepared for electron microscopy. The ages of the monkeys ranged from 5 to 35 years, covering the entire adult life span of this species. A total of 140 Betz Cell profiles (20 per monkey) were examined. Measurements of these profiles confirmed our earlier finding of a decline in the perimeters of Betz Cell somata with advancing age. The 1,540 axon terminals upon these Cells, however, remained unchanged in size and length of membrane apposition, as well as in their number of mitochondria throughout the adult life (greater than or equal to 5 years) of the rhesus monkey. In addition, the total number of axon terminals on Betz Cells did not change with age. Because the axosomatic terminals showed no age-associated changes, the material was used to calculate parametric characteristics of Betz Cells and associated terminals. Betz Cell somata of the rhesus monkey were estimated to have a mean membrane surface area of 5,700 microns2. Axosomatic terminals on Betz Cell somata had a mean appositional area of about 3.33 microns2 and covered about 15% of the somal surface. Thus, on average, each Betz Cell appeared to receive approximately 260 axosomatic terminals. There were also some conspicuous age-associated changes in the motor cortex that were not quantified. These included an accumulation of lipofuscin and the presence of a novel inclusion body in the somata of Betz Cells. Age-related occurrences in the neuropil included the degeneration of axons and their myelin, membrane-bound holes, and neuritic (senile) plaques.
Mirco Cosottini - One of the best experts on this subject based on the ideXlab platform.
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Semiautomated Evaluation of the Primary Motor Cortex in Patients With Amyotrophic Lateral Sclerosis at 3T
American Journal of Neuroradiology, 2017Co-Authors: Graziella Donatelli, Alessandra Retico, E. Caldarazzo Ienco, Paolo Cecchi, Mauro Costagli, Daniela Frosini, Laura Biagi, Michela Tosetti, Gabriele Siciliano, Mirco CosottiniAbstract:BACKGROUND AND PURPOSE: Amyotrophic lateral sclerosis is a neurodegenerative disease involving the upper and lower motor neurons. In amyotrophic lateral sclerosis, pathologic changes in the primary motor cortex include Betz Cell depletion and the presence of reactive iron-loaded microglia, detectable on 7T MR images as atrophy and T2*-hypointensity. Our purposes were the following: 1) to investigate the signal hypointensity-to-thickness ratio of the primary motor cortex as a radiologic marker of upper motor neuron involvement in amyotrophic lateral sclerosis with a semiautomated method at 3T, 2) to compare 3T and 7T results, and 3) to evaluate whether semiautomated measurement outperforms visual image assessment. MATERIALS AND METHODS: We investigated 27 patients and 13 healthy subjects at 3T, and 19 patients and 18 healthy subjects at 7T, performing a high-resolution 3D multiecho T2*-weighted sequence targeting the primary motor cortex. The signal hypointensity-to-thickness ratio of the primary motor cortex was calculated with a semiautomated method depicting signal intensity profiles of the cortex. Images were also visually classified as “pathologic” or “nonpathologic” based on the primary motor cortex signal intensity and thickness. RESULTS: The signal hypointensity-to-thickness ratio of the primary motor cortex was greater in patients than in controls ( P P CONCLUSIONS: The signal hypointensity-to-thickness ratio of the primary motor cortex calculated with a semiautomated method is suggested as a radiologic marker of upper motor neuron burden in patients with amyotrophic lateral sclerosis. This semiautomated method may be useful for improving the subjective radiologic evaluation of upper motor neuron pathology in patients suspected of having amyotrophic lateral sclerosis.
Jae-wook Yoo - One of the best experts on this subject based on the ideXlab platform.
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A Case of Severe Brain Atrophy Found in the Man in His Twenties Who Drinks Moderate Amount of Alcohol
2016Co-Authors: Jae-wook Yoo, Jong-soon ChoiAbstract:Brain atrophy is caused by the neuronal loss and reduction in Betz Cell numbers. Among the many causes of brain atrophy, alcohol related atrophy is largely accounted for by a reduction in white matter volume. And the degree of brain atrophy correlates with the rate and amount of alcohol consumed over a lifetime, and it is at least partially reversible with alcohol abstinence. Alcohol-related brain damage mechanism correlates with that ethanol selectively and potently inhibits the function of NMDA receptors. Chronic alcoholics often have a low intake of folate, hence a sustained hyperhomocystenemia can frequently be observed, then this cause a pathological increase in receptor activity and subsequent excitotoxic damage. Even the consumption of light and moderate doses of alcohol lead to shrinkage of the brain and to increases in white matter volume and decrease in grey matter volume. We report the case of severe brai
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A Case of Severe Brain Atrophy Found in the Man in His Twenties Who Drinks Moderate Amount of Alcohol
Korean Journal of Family Medicine, 2010Co-Authors: Jae-wook Yoo, Jong-soon ChoiAbstract:Brain atrophy is caused by the neuronal loss and reduction in Betz Cell numbers. Among the many causes of brain atrophy, alcohol related atrophy is largely accounted for by a reduction in white matter volume. And the degree of brain atrophy correlates with the rate and amount of alcohol consumed over a lifetime, and it is at least partially reversible with alcohol abstinence. Alcohol-related brain damage mechanism correlates with that ethanol selectively and potently inhibits the function of NMDA receptors. Chronic alcoholics often have a low intake of folate, hence a sustained hyperhomocystenemia can frequently be observed, then this cause a pathological increase in receptor activity and subsequent excitotoxic damage. Even the consumption of light and moderate doses of alcohol lead to shrinkage of the brain and to increases in white matter volume and decrease in grey matter volume. We report the case of severe brain atrophy incidentally found at medical check-up in a young man who has drunken alcohol too much for 10 years.