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Biomedical subjects

J J Kril

Publications and source records attributed to J J Kril.

13 recordsLinked to original sources
PubMed1992

Amino acid neurotransmitter receptor changes in cerebral cortex in alcoholism: effect of cirrhosis of the liver.

Gamma-aminobutyric acidA/benzodiazepine receptor binding sites and the N-methyl-D-aspartate subclass of glutamate receptor sites were assessed in synaptic plasma membrane homogenates of cerebral cortex tissue obtained at autopsy from cirrhotic and noncirrhotic alcoholic patients and matched control subjects. The alcoholic patients consumed an average of greater than 80 g of ethanol/day, the control subjects less than 20 g/day. Postmortem delays up to approximately 100 h caused no significant loss of any of the binding sites; the patient and subject groups were closely matched for age. The affinities (KD) of the receptor sites did not differ between the patient and subject groups, nor between cortical regions. Using three different radioligands ([3H]muscimol, [3H]flunitrazepam, and [3H]diazepam), the gamma-aminobutyric acidA/benzodiazepine receptor complex was found to have greater density (Bmax) in superior frontal gyrus in alcoholic patients (which selectively shows morphological change in alcoholic patients), but was unchanged in motor cortex. Alcoholic patients with cirrhosis had much less pronounced changes. The density of the N-methyl-D-aspartate subclass of glutamate receptors, assessed with [3H]MK-801, did not vary across patient and subject groups.

Adult↗
PubMed1991

Increased central immunoreactive beta-endorphin content in patients with Wernicke-Korsakoff syndrome and in alcoholics.

beta-endorphin, adrenocorticotrophin, and alpha-melanocyte stimulating hormone were measured by radioimmunoassay in three areas of human brain at necropsy in seven subjects with Wernicke-Korsakoff syndrome and in 52 controls. Thiamin concentration in six brain areas was also measured. Mamillary body beta-endorphin concentrations were significantly increased in those with the syndrome compared with controls, and those controls with high alcohol intake showed increased mamillary body beta-endorphin compared with controls with low alcohol intake. Brain thiamin concentration was similar in both groups, with the exception of the brainstem, where it was reduced in subjects with Wernicke-Korsakoff syndrome. Thalamic beta-endorphin in controls was inversely correlated with thiamin in frontal white matter, frontal cortex, parietal white matter and parietal cortex, while beta-endorphin in the hypothalamus of patients was inversely correlated with thiamin in frontal cortex, parietal white matter, thalamus and brainstem. These results suggest that there is a disturbance of the endorphinergic system in Wernicke-Korsakoff syndrome which may be related to alcohol intake.

Adrenocorticotropic Hormone↗
PubMed1990

Neuropathology of alcoholism.

There are wide ranging effects of alcohol on the nervous system. Some interfere with physiological and neurochemical functions but ultimately structural damage occurs. During life one of the most impressive changes is brain shrinkage which can be visualized using neuroradiological imaging techniques. This article reviews the pathological explanations for brain shrinkage and addresses the question of the pathogenesis of the reversible component of this damage in relation to prolonged abstinence from alcohol. This shrinkage seems to relate to a loss of white matter. However, the cortex is also abnormal in that there is a loss of neurones from the frontal region. In this and other regions of the cortex examined there is shrinkage of the neuronal soma. This is reflected in a retraction of the neuronal dendritic arbor which plays a crucial role in cell-to-cell communication. In addition, the cerebellum appears to be vulnerable in alcoholic patients although it may well be that associated nutritional deficiencies play an important role. The Wernicke-Korsakoff syndrome is another important deficiency disorder which is seen most frequently in alcoholic patients. Two important population groups which are considered in this review are females and moderate ('social') drinkers. Females are thought to be more susceptible to the damaging effects of alcohol than males and this is examined in the light of the scant data available. Similarly, there are few neuropathological data on people who drink 30-80 grams of alcohol per day. In order to assess so-called 'safe levels of drinking' this is an important group to study.

Alcohol Amnestic Disorder↗
PubMed1990

Brain and liver dolichol in chronic alcoholism: a necropsy study.

Cerebral gray and white matter and liver dolichol levels were measured in postmortem samples from chronic alcoholics and nonalcoholic controls following recent suggestions that dolichol levels may be used as a marker for alcoholism. No significant differences in brain dolichol were found between the control and alcoholic groups. A significant reduction in the liver dolichol was observed in the alcoholic group. This was most marked in those alcoholics with liver disease.

Adult↗
PubMed1990

The effects of alcohol on the female brain: a neuropathological study.

This quantitative neuropathological study compared the brains of seventeen alcoholic females with twenty non-alcoholic female controls. There was a significant (P less than 0.001) increase in the pericerebral space value (control 9.5; alcoholic 16.3) indicating shrinkage of the brain. Cerebral grey and white matter volumes were determined morphometrically. There was a significant decrease in the cerebral white matter volume (P less than .02) in the alcoholics. The cerebral grey matter volume was unchanged. These changes parallel those described previously in male alcoholics. Further studies will be necessary to establish the relative severity of the brain damage in males and females.

Alcohol Drinking↗
PubMed1989

Cortical dihydropyridine binding sites are unaltered in human alcoholic brain.

The density and affinity of sites labeled by the 1,4-dihydropyridines, [3H]nitrendipine and (+) [3H]PN 200-110, were not significantly different in superior frontal and parietal cortical membranes from alcoholic patients and nonalcoholic control patients. This is in contrast to the increased number of dihydropyridine receptors and increased functional activity of calcium channels reported in brain from rats treated chronically with ethanol and in neural cell lines grown in the presence of ethanol. These results indicate that 1,4-dihydropyridine-sensitive calcium channels (L type) in the brain, despite possible acute changes, are unaltered following long-term ethanol exposure in humans.

Alcoholism↗
PubMed1989

Neuronal counts from four cortical regions of alcoholic brains.

Neuronal loss from the frontal superior cortex of the brains of alcoholics has recently been documented. In addition to this, a reduction in the mean neuronal area was also seen in the frontal and motor cortices. This suggested a regional specificity of neuronal damage in the brains of alcoholics. Further quantitation of other cortical regions of the same cases as used in the above study has been performed. The frontal cingulate and temporal cortices were examined and there was found to be no significant alteration in the number of neurons when compared to a control population. There was, however, a significant reduction in the mean size of the neuronal soma in the frontal cingulate cortex (P less than 0.05). These data support the hypothesis of regional variations in the severity of cerebral cortical damage in alcoholism with shrinkage of neurons in most regions examined but neuronal loss only in the superior frontal gyrus.

Adult↗
PubMed1988

Brain shrinkage in alcoholics is not caused by changes in hydration: a pathological study.

Measurement of the water content of the cerebral white matter in 26 control and 24 alcoholic cases supports in vivo MRI studies and previous necropsy studies which appeared to show an increase in the water content in the alcoholic group. This negates the hypothesis that reversible brain shrinkage in alcoholics is caused by changes in the state of hydration.

Aged↗
PubMed1988

Necropsy study of GABA/benzodiazepine receptor binding sites in brain tissue from chronic alcoholic patients.

Neurological and cognitive deficits occur in many chronic alcoholic patients. Quantitative studies reveal a significant reduction in the number of neurons in the superior frontal gyrus of chronic alcoholics, with no change in the motor cortex. Our studies are aimed at delineating which neurotransmitter systems are altered in alcoholics and to correlate these alterations with morphometry and, where possible, clinical signs. Much evidence suggests both short- and long-term effects of ethanol on GABA-mediated neurotransmission. GABA and benzodiazepines bind to distinct, but allosterically linked, sites on the GABA/benzodiazepine receptor complex. In the absence of any detected difference in the number of benzodiazepine receptors in both the frontal and motor cortex from alcoholic and control patients, a significant increase in the amount of GABA enhancement of [3H]diazepam binding was measured in frontal cortex membranes from patients with Wernicke's encephalopathy relative to non-alcoholic controls. This finding suggests an increased coupling of the GABA and benzodiazepine recognition sites in this area, which may be due to ethanol-induced conformational changes in the receptor complex.

Alcoholism↗
PubMed1985

Brain shrinkage in chronic alcoholics: a pathological study.

A quantitative neuropathological necropsy study of 22 control and 22 chronic alcoholic subjects showed a statistically significant loss of brain tissue in the chronic alcoholic group. The loss of tissue appeared to be from the white matter of the cerebral hemispheres rather than the cerebral cortex. This may reflect a primary alteration in the composition or structure of the white matter or it may be secondary to loss of nerve cells from the cortex with subsequent degeneration of the axons in the white matter. Further morphometric analyses including cortical neuronal counts will be necessary to clarify this issue.

Adolescent↗