Disease relevance of Korsakoff Syndrome

• Alcohol-related illness before the index treatment played an important role: the mortality rate was higher for those who had had Wernicke-Korsakoff syndrome (40%), delirium tremens (15.3%), pancreatitis (13.9%) or cardiomyopathy (14.1%) [1].
• AIMS: To investigate a possible relationship between cerebellar glucose metabolism and recovery from ataxia in the first months of acute Wernicke-Korsakoff syndrome [2].
• It is suggested that failure to ensure that head injury patients at risk of Wernicke-Korsakoff syndrome receive appropriate thiamine prophylaxis represents a missed and treatable additional insult to the damaged brain [3].
• Hypothermia and coma in the Wernicke-Korsakoff syndrome [4].
• Hyperemesis gravidarum can induce Wernicke-Korsakoff syndrome (WKS), a thiamin deficiency disorder characterized by ocular abnormalities, ataxia and disturbance of consciousness [5].

Psychiatry related information on Korsakoff Syndrome

• No association between DLST gene and Alzheimer's disease or Wernicke-Korsakoff syndrome [6].
• Results from our study indicate that the following measures are mandatory: educating patients about proper dietary habits, carefully monitoring their thiamin intake, recognizing Wernicke-Korsakoff syndrome early, and treating it immediately with appropriate measures [7].
• Evidence that patients with the Wernicke-Korsakoff syndrome have an altered thiamin-requiring isoenzyme and evidence that six patients with Wernicke's encephalopathy failed to respond to oral thiamin has caused some doubt as to whether the target population would be able to benefit from the measure [8].
• The preliminarily findings of this study with 16 patients suggested that memantine is effective in the treatment of dementia in Wernicke-Korsakoff syndrome [9].

High impact information on Korsakoff Syndrome

• The Wernicke-Korsakoff syndrome is a thiamine-deficiency disorder occurring primarily among alcoholics [10].
• Our data suggest that an inborn error (i.e., high Km of transketolase for thiamine pyrophosphate) predisposing to thiamine deficiency diseases similar to those reported in Wernicke-Korsakoff syndrome may occur in the general population [11].
• Coma in the Wernicke-Korsakoff syndrome [12].
• Vasopressin and memory in Korsakoff syndrome [13].
• Variants of the enzyme transketolase which possess reduced affinity for its cofactor thiamine pyrophosphate (high apparent Km) have been described in chronic alcoholic patients with Wernicke-Korsakoff syndrome [14].

Chemical compound and disease context of Korsakoff Syndrome

• Pyrithiamine is an inhibitor of thiamine metabolism that induces neurological symptoms similar to that of Wernicke-Korsakoff Syndrome in animals [15].
• "Grievous bodily harm:" gamma hydroxybutyrate abuse leading to a Wernicke-Korsakoff syndrome [16].
• Results of this study demonstrate significant reductions of TPP-dependent enzymes [pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase (alpha KGDH), and transketolase] in autopsied cerebellar vermis samples from alcoholic patients with the clinical and neuropathologically confirmed diagnosis of Wernicke-Korsakoff Syndrome (WKS) [17].
• Impaired melatonin secretion in patients with Wernicke-Korsakoff syndrome [18].
• Alcohol and aldehyde dehydrogenase genotypes in Korsakoff syndrome [19].

Biological context of Korsakoff Syndrome

• Thus, allelic variants of the transketolase gene cannot account for the biochemically distinct forms of the enzyme found in these patients nor be considered as a mechanism for genetic predisposition to the development of Wernicke-Korsakoff syndrome [14].
• Quantitative receptor autoradiography was used to evaluate the density of high-affinity binding sites for the "peripheral-type" benzodiazepine receptor (PTBR) ligand [3H]PK11195 in brain regions of the rat at different stages of pyrithiamine-induced thiamine deficiency encephalopathy, an experimental model of the Wernicke-Korsakoff syndrome (WKS) [20].
• Thiamin deficiency and prevention of the Wernicke-Korsakoff syndrome. A major public health problem [21].
• Molecular genetics of transketolase in the pathogenesis of the Wernicke-Korsakoff syndrome [22].

Anatomical context of Korsakoff Syndrome

• We studied a thiamine-requiring enzyme in cultured cells from four patients with the Wernicke-Korsakoff syndrome to determine whether these patients have a genetic predilection to thiamine deficiency [23].
• Erythrocyte transketolase activity in the Wernicke-Korsakoff syndrome [24].

Gene context of Korsakoff Syndrome

• Apolipoprotein E epsilon 4 allele distribution in Wernicke-Korsakoff syndrome with or without global intellectual deficits [25].
• Transketolase is a key enzyme in the pentose-phosphate pathway which has been implicated in the latent human genetic disease, Wernicke-Korsakoff syndrome [26].
• Forty-seven per cent of patients received "stat" intravenous thiamine (although the Wernicke-Korsakoff syndrome is rare) [27].

Analytical, diagnostic and therapeutic context of Korsakoff Syndrome

• The majority of psychiatrists favoured oral administration for prophylaxis against the Wernicke-Korsakoff syndrome in chronic alcohol misusers and parenteral therapy in patients with signs of Wernicke-Korsakoff syndrome [28].

References