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  • glutamate  (7)
  • Hepatic encephalopathy  (4)
  • Thiamine deficiency  (3)
  • manganese  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Pathophysiology of alcoholic brain damage: synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease (1995)
    Springer
    Metabolic brain disease 10 (1995), S. 1-8 
    Details
    ISSN: 1573-7365
    Keywords: Alcoholic brain damage ; Ethanol neurotoxicity ; Thiamine deficiency ; Alcoholic liver disease ; Hepatic Encephalopathy ; Cerebral energy deficit ; NMDA receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chronic alcoholism results in brain damage and dysfunction leading to a constellation of neuropsychiatric symptoms including cognitive dysfunction, the Wernicke-Korsakoff Syndrome, alcoholic cerebellar degeneration and alcoholic dementia. That these clinically-defined entities result from independent pathophysiologic mechanisms is unlikely. Alcohol and its metabolite acetaldehyde are directly neurotoxic. Alcoholics are thiamine deficient as a result of poor diet, gatrointestinal disorders and liver disease. In addition, both alcohol and acetaldehyde have direct toxic effects on thiamine-related enzymes in liver and brain. Alcoholics frequently develope severe liver disease and liver diseaseper se results in altered thiamine homeostasis, in cognitive dysfunction and in neuropathologic damage to astrocytes. The latter may result in the loss of neuron-astrocytic trafficking of neuroactive amino acids and thiamine esters, essential to CNS function. The present review article proposes mechanisms whereby the effects of alcohol, thiamine deficiency and liver disease combine synergistically to contribute to the phenomena of cognitive dysfunction and “alcoholic brain damage”.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01991777
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  • 2
    Electronic Resource
    Electronic Resource
    Neuroactive amino acids in hepatic encephalopathy (1996)
    Springer
    Metabolic brain disease 11 (1996), S. 165-173 
    Details
    ISSN: 1573-7365
    Keywords: Hepatic encephalopathy ; Amino acids ; Glutamate ; GABA ; Taurine ; Endogenous benzodiazepines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is abundant evidence to suggest that alterations of excitatory and inhibitory amino acids play a significant role in the pathogenesis of hepatic encephalopathy (HE) in both acute and chronic liver diseases. Brain glutamate concentrations are reduced in patients who died in hepatic coma as well as in experimental HE, astrocytic reuptake of glutamate is compromised in liver failure and postsynaptic glutamate receptors (both NMDA and non-NMDA subclasses) are concomitantly reduced in density. Recent studies in experimental acute liver failure suggest reduced capacity of the astrocytic glutamate transporter in this condition. Together, this data suggests that neuron-astrocytic trafficking of glutamate is impaired in HE. Other significant alterations of neuroactive amino acids in HE include a loss of taurine from brain cells to extracellular space, a phenomenon which could relate both to HE and to brain edema in acute liver failure. Increased concentrations of benzodiazepine-like compounds have been reported in human and experimental HE. Clinical trials with the benzodiazepine antagonist flumazenil reveal a beneficial effect in some patients with HE; the mechanism responsible for this effect, however, remains to be determined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02069503
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  • 3
    Electronic Resource
    Electronic Resource
    Activities of neuronal and astrocytic marker enzymes in autopsied brain tissue from patients with hepatic encephalopathy (1987)
    Springer
    Metabolic brain disease 2 (1987), S. 283-290 
    Details
    ISSN: 1573-7365
    Keywords: hepatic encephalopathy ; glutamic acid decarboxylase ; glutamine synthetase ; choline acetyltransferase ; autopsied brain tissue ; γ-aminobutyric acid (GABA) ; glutamate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Activities of the γ-aminobutyric acid (GABA) and cholinergic nerve-terminal marker enzymes glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT) as well as the astrocytic enzyme glutamine synthetase (GS) were measured in homogenates of dissected brain tissue obtained at autopsy from nine cirrhotic patients dying in hepatic encephalopathy and an equal number of control subjects matched for age, agonal status, and time interval from death to freezing of autopsied material. GAD activities varied as a function of agonal status in control samples, confirming a previous report, but were unchanged in brain tissue from cirrhotic patients, suggesting no loss of integrity of presynaptic GABA nerve terminals in this disease. On the other hand, GS activities were selectively decreased by 25% (P 〈 0.01) in caudate nuclei of cirrhotic patients, reflecting, no doubt, the severe astrocytosis consistently observed in this brain structure. CAT activities, expressed per milligram of protein, were found to be increased by 30% (P 〈 0.01) in the prefrontal cortex of cirrhotic patients. Whether such changes result from a relative increase in CAT as a consequence of losses of astrocytic protein or reflect altered cholinergic function in hepatic encephalopathy associated with chronic liver disease awaits further study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999698
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  • 4
    Electronic Resource
    Electronic Resource
    Densities of binding sites for the “peripheral-type” benzodiazepine receptor ligand3H-PK11195 are increased in brain 24 hours following portacaval anastomosis (1994)
    Springer
    Metabolic brain disease 9 (1994), S. 267-273 
    Details
    ISSN: 1573-7365
    Keywords: Portacaval anastomosis ; Hepatic encephalopathy ; 3H-PK11195 binding ; “Peripheral-type” benzodiazepine receptor ; Astrocyte ; Portal-systemic encephalopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Quantitative receptor autoradiography was used to measure the densities of binding sites for the “peripheral-type” benzodiazepine receptor ligand3H-PK11195 in regions of the rat brain 1, 3, 7 and 28 days following portacaval anastomosis (PCA) and in sham-operated control animals. The results demonstrate that densities of3H-PK11195 binding sites were significantly increased in the cerebral cortex (by 40%, p〈0.05) as early as 24 hours following PCA. In the thalamus significant increases in densities of3H-PK11195 binding sites were seen 3 days after PCA, whereas in brain regions such as the striatum and cerebellum, significant increases in3H-PK11195 binding sites were not evident until 7 days following PCA. By 28 days following PCA increased densities of3H-PK11195 binding sites were well established and widespread throughout the brain. Previous studies demonstrate early increases of brain ammonia following. PCA. PTBRs or their endogenous ligands could play an important role in the early astrocytic response (mitochondrial proliferation, swelling) to ammonia following PCA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01991200
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  • 5
    Electronic Resource
    Electronic Resource
    Cerebral aminoacids in portal-systemic encephalopathy: Lack of evidence for altered γ-aminobutyric acid (GABA) function (1986)
    Springer
    Metabolic brain disease 1 (1986), S. 221-228 
    Details
    ISSN: 1573-7365
    Keywords: hepatic encephalopathy ; portal-systemic encephalopathy ; portocaval anastomosis ; glutamine ; glutamate ; γ-aminobutyric acid ; hyperammonemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Construction of an end-to-side portocaval anastomosis in the rat resulted, 4 weeks later, in sustained hyperammonemia and two- to threefold increases in brain ammonia. Measurement of cerebral amino acids using a sensitive double-isotope dansyl microtechnique revealed substantial increases in the glutamine content of cerebral cortex and brain stem. Glutamate levels were found to be concomitantly reduced in both brain regions compared to those of sham-operated controls. The γ-aminobutyric acid (GABA) content of cerebral cortex and brain stem was unaffected by portocaval shunting, as were activities of the GABA nerveterminal marker enzyme glutamic acid decarboxylase (GAD). These findings suggest that impaired GABA function may not play a major role in the pathogenesis of hepatic encephalopathy associated with portocaval shunts. Preliminary evidence suggests that decreased cerebral glutamate may reflect its loss from the releasable (neurotransmitter) pool.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01001783
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  • 6
    Electronic Resource
    Electronic Resource
    Manganese toxicity, dopaminergic dysfunction and hepatic encephalopathy (1995)
    Springer
    Metabolic brain disease 10 (1995), S. 259-267 
    Details
    ISSN: 1573-7365
    Keywords: manganese ; hepatic encephalopathy ; MR signal hyperintensity ; globus pallidus ; dopamine D2 receptors ; MAO ; extrapyramidal symptoms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Patients with chronic liver disease manifest a high incidence (〉75%) of pallidal signal hyperintensity on T1-weighted Magnetic Resonance Imaging (MRI), the intensity of which correlates with blood manganese levels and the presence of extrapyramidal symptoms. A major cause of pallidal hyperintensity on T1-weighted MRI is manganese deposition; chronic manganese intoxication in the absence of liver disease results in pallidal MR signal hyperintensity, in extrapyramidal symptoms and in selective effects on the dopaminergic neurotransmitter system in basal ganglia. Direct measurements in globus pallidus obtained at autopsy from patients with chronic liver disease who died in hepatic coma reveal 2 to 7-fold increases of pallidal manganese and a concomitant loss of dopamine D2 binding sites. Liver transplantation results in normalization of pallidal MR signals and of blood manganese levels. These findings suggest that (1) pallidal MR signal hyperintensity in patients with chronic liver disease is the result of manganese deposition and (2) alterations of dopaminergic function due to the toxic effects of manganese may contribute to the extrapyramidal symptoms in these patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02109357
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  • 7
    Electronic Resource
    Electronic Resource
    Accumulation of manganese and copper in pallidum of cirrhotic patients: role in the pathogenesis of hepatic encephalopathy? (1995)
    Springer
    Metabolic brain disease 10 (1995), S. 353-356 
    Details
    ISSN: 1573-7365
    Keywords: Hepatic encephalopathy ; manganese ; copper ; zinc ; globus pallidus ; liver disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Concentrations of zinc, copper and manganese were measured by atomic absorption spectrometry in samples of globus pallidus obtained at autopsy from 9 patients with chronic liver disease and an equal number of age-matched controls. Manganese concentrations were significantly increased several fold (p〈0.01) in globus pallidus of liver disease patients accompanied by smaller but significant 2-fold increases of copper. Zinc concentrations, on the other hand, were within normal limits. Increased pallidal manganese offers a cogent explanation for the observed T1-weighted MRI signal hyperintensity in pallidum of cirrhotic patients. Increased copper content in brain suggests the existence of common pathophysiologic mechanisms in inherited (Wilson Disease) and acquired hepatocerebral disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02109365
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  • 8
    Electronic Resource
    Electronic Resource
    Alterations of Neurotransmitter-Related Gene Expression in Human and Experimental Portal-Systemic Encephalopathy (1998)
    Springer
    Metabolic brain disease 13 (1998), S. 337-349 
    Details
    ISSN: 1573-7365
    Keywords: Portal-systemic encephalopathy ; hepatic encephalopathy ; ammonia ; manganese ; gene expression ; peripheral-type benzodiazepine receptors ; monoamine oxidase ; serotonin ; neurosteroids ; nitric oxide synthase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Portal-systemic encephalopathy (PSE) is a serious neuropsychiatric condition that results from chronic liver failure and portal-systemic shunting of venous blood. PSE is particularly prevalent following treatment of portal hypertension or ascites by the TIPS procedure. Recent studies both in autopsied brain tissue from PSE patients as well as in experimental animal models of PSE reveal that chronic liver failure results in altered expression of several genes coding for proteins having key roles in the control of neuronal excitability. Such alterations include increased expression of monoamine oxidase (MAO-A isoform), the “peripheral-type” benzodiazepine receptor (PTBR) as well as constitutive, neuronal nitric oxide synthase (nNOS). Such changes result in altered protein expression and in increased degradation of monoamine neurotransmitters, increased synthesis of neurosteroids with inhibitory properties and increased production of nitric oxide (respectively) in brain in chronic liver failure. In the case of PTBR and nNOS, increases in expression result from exposure to ammonia and/or manganese, two neurotoxic agents shown previously to be increased in brain in chronic liver failure. Further elucidation of the consequences of neurotransmitter-related gene expression could identify new pathophysiologic mechanisms and result in new approaches to the prevention of PSE in chronic liver disease in humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020641009971
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  • 9
    Electronic Resource
    Electronic Resource
    Thiamine-dependent enzyme changes in temporal cortex of patients with Alzheimer's disease (1990)
    Springer
    Metabolic brain disease 5 (1990), S. 179-184 
    Details
    ISSN: 1573-7365
    Keywords: Alzheimer's disease ; thiamine-dependent enzymes ; thiamine ; vitamin B1 ; pyruvate dehydrogenase complex ; α-ketoglutarate dehydrogenase ; transketolase ; glutamate ; dehydrogenase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Activites of thiamine-dependent enzymes [pyruvate dehydrogenase (PDHC), α-ketoglutarate dehydrogenase (αKGDH), and transketolase (TK)] were measured in autopsied samples of temporal cortex from six patients with Alzheimer's disease and from eight age-matched control subjects who were free from neurological or psychiatric diseases. Times from death to freezing of dissected material at −70°C were matched. Significant decreases in PDHC (decreased by 70%;P〈0.01), αKGDH (decreased by 70%; p〈0.01), and TK (decreased by 52%;P〈0.01) were observed in brain tissue from patients with Alzheimer's disease. In contrast, activities of glutamate dehydrogenase were within normal limits. These findings suggest a possible role for alterations of brain thiamine metabolism or utilization in Alzheimer's disease
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00997071
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  • 10
    Electronic Resource
    Electronic Resource
    Pyrithiamine-induced thiamine deficiency results in decreased Ca2+-dependent release of glutamate from rat hippocampal slices (1991)
    Springer
    Metabolic brain disease 6 (1991), S. 125-132 
    Details
    ISSN: 1573-7365
    Keywords: thiamine deficiency ; pyrithiamine ; glutamate release ; glutamate ; hippocampal slice ; Wemicke's encephalopathy ; Wemicke-Korsakoff syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alterations of excitatory amino acids in brain may be of pathophysiological significance in thiamine-deficiency encephalopathy. The present study was undertaken to evaluate the effects of thiamine deficiency induced by the central thiamine antagonist, pyrithiamine, on the glutamate content of glutamatergic nerve terminals. Electrically-stimulated, Ca2+-dependent release of glutamate from hippocampal slices obtained from symptomatic pyrithiamine-treated rats was significantly decreased compared to pair-fed controls. Possible explanations for the decreased “neurotransmitter pool” of glutamate in thiamine-deficient rat brain include decreased synthesis of glutamate as a result of decreased activities of the thiamine-dependent enzyme α-ketoglutarate dehydrogenase or increased release of glutamateper se. There is evidence to suggest that the latter mechanism with ensuing excitotoxic neuronal damage could be involved in the pathogenesis of selective neuronal death in thiamine deficiency. Similar mechanisms could be implicated in Wemicke's encephalopathy in humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00996904
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