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  • 1
    ISSN: 1573-7365
    Keywords: Alcohol ; serotonin ; neuropathology ; median raphe nucleus ; Wernicke-Korsakoff ; cirrhosis ; thiamine deficiency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have identified alcohol, thiamine deficiency and liver disease as contributing to the neuropathology of alcohol-related brain damage. In order to examine the effects of alcohol toxicity and thiamine deficiency on serotonergic neurons in the median raphe nucleus (MnR), alcoholic and previously published Wernicke-Korsakoff syndrome (WKS) cases without liver disease, were compared with age-matched non-alcoholic controls. While there was no difference between the estimated number of serotonergic neurons in either controls or alcoholics without WKS (means of 63,010±8,900 and 59,560±8,010 respectively), a substantial loss of serotonergic neurons was previously found in WKS cases (mean of 19,050±13,140). Further analysis revealed a significant difference in the maximum daily alcohol consumption between these groups. However, analysis of covariance showed that the number or serotonergic neurons in the MnR did not correlate with the amount of alcohol consumed. Therefore, our results suggest that cell loss in the MnR can be attributed to thiamine deficiency rather than alcoholper se.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Metabolic brain disease 10 (1995), S. 81-91 
    ISSN: 1573-7365
    Keywords: Neurofibrillary tangles ; peroxidase activity ; nucleus basalis ; thiamine deficiency ; alcohol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tau immunoreactivity was examined in post mortem tissue from patients in three groups: neurologically-asymptomatic and neuropathologically normal alcoholics, alcoholics with Wernicke's Encephalopathy (WE) and age matched non-alcoholic controls. Tau-positive granular and fibrillary inclusions were frequently observed within the magnocellular neurons of the cholinergic nucleus basalis, within occasional nucleus basalis neurons in non-WE alcoholics, but not in controls. Tau immunoreactivity was not however observed in cortical, brainstem, diencephalic or non-cholinergic forebrain structures. Peroxidase activity was also examined within the nucleus basalis using diaminobenzidine as an indicator. The majority of neurons in the basal forebrain showed increased peroxidase activity in all WE alcoholics and in some nucleus basalis neurons of non-WE alcoholics, but was rarely seen in controls. Neighboring astrocytes also showed increased peroxidase activity. These results suggest a link between peroxidase activity and the abnormal accumulation of phosphorylated tau. The presence of tau in the nucleus basalis of alcoholics with WE suggests a thiamine-dependent mechanism in tau accumulation and cell death in the cholinergic basal forebrain.
    Type of Medium: Electronic Resource
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