Increased histamine release and granulocytes within the thalamus of a rat model of Wernicke's encephalopathy

McRee, R; Terry-Ferguson, Melissa; Langlais, Philip J.; Chen, Y; Nalwalk, Julia W.; Blumenstock, Frank A.; Hough, Lindsay B.

doi:10.1016/s0006-8993(99)02309-4

Cited by 20 publications

(15 citation statements)

References 55 publications

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“…Animal models support a contribution of classical sterile neuroinflammatory mechanisms (cf., Graeber et al, 2011) in thiamine deficiency related pathology. Indeed, neuropathologic consequences of thiamine deficiency include blood-brain barrier breakdown (Beauchesne et al, 2009; Calingasan and Gibson, 2000; Ke and Gibson, 2004; Nixon et al, 2008) and accumulation of innate and adaptive immune cells in CNS tissue (McRee et al, 2000; Meng and Okeda, 2003). Alterations in glial cell morphology were reported in early studies of experimental thiamine deficiency (Collins, 1967; Robertson et al, 1968; Tellez and Terry, 1968) and in human WE (Victor et al, 1971).…”

Section: Introductionmentioning

confidence: 99%

Associations between in vivo neuroimaging and postmortem brain cytokine markers in a rodent model of Wernicke's encephalopathy

Zahr

Alt

Mayer

et al. 2014

Experimental Neurology

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Thiamine (vitamin B1) deficiency, associated with a variety of conditions, including chronic alcoholism and bariatric surgery for morbid obesity, can result in the neurological disorder Wernicke’s encephalopathy (WE). Recent work building upon early observations in animal models of thiamine deficiency has demonstrated an inflammatory component to the neuropathology observed in thiamine deficiency. The present, multilevel study including in vivo magnetic resonance imaging (MRI) and spectroscopy (MRS) and postmortem quantification of chemokine and cytokine proteins sought to determine whether a combination of these in vivo neuroimaging tools could be used to characterize an in vivo MR signature for neuroinflammation. Thiamine deficiency for 12 days was used to model neuroinflammation; glucose loading in thiamine deficiency was used to accelerate neurodegeneration. Among 38 animals with regional brain tissue assayed postmortem for cytokine/chemokine protein levels, three groups of rats (controls+glucose, n=6; pyrithiamine+saline, n=5; pyrithiamine+glucose, n=13) underwent MRI/MRS at baseline (time 1), after 12 days of treatment (time 2), and 3h after challenge (glucose or saline, time 3). In the thalamus of glucose-challenged, thiamine deficient animals, correlations between in vivo measures of pathology (lower levels of N-acetyle aspartate and higher levels of lactate) and postmortem levels of monocyte chemotactic protein-1 (MCP-1, also known as chemokine ligand 2, CCL2) support a role for this chemokine in thiamine deficiency-related neurodegeneration, but do not provide a unique in vivo signature for neuroinflammation.

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Section: Introductionmentioning

confidence: 99%

Associations between in vivo neuroimaging and postmortem brain cytokine markers in a rodent model of Wernicke's encephalopathy

Zahr

Alt

Mayer

et al. 2014

Experimental Neurology

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“…A perivascular inflammatory response and increased blood-brain barrier permeability [9,10] contribute to neuronal damage and radiological changes, probably in the advanced phases.…”

Section: Discussionmentioning

confidence: 99%

Dramatic Recovery from Prolonged Wernicke-Korsakoff Disease

Carota¹,

Schnider²

2004

Eur Neurol

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“…They established that the histamine enhancement of glutamate receptor activation suggests that the histamine release could be a participant in glutamate-N-methyl-D-aspartate (NMDA)-mediated excitotoxic neuronal death in this pathology (Langlais et al, 1994). And, that the release of histamine in rat from nerve terminals and histamine and other vasoactive substances from granulocytes could be responsible for thiamine deficiencyinduced vascular breakdown and perivascular edema in thalamus (McRee et al, 2000). Espey et al (1998) determined in mice infected with LP-BM5 leukemia retrovirus mixture that develop a progressive immunodeficiency with associated behavioral, histological, and neurochemical alterations consistent with glutamatergic hyperactivation.…”

Section: Thiamine Deficiency Encephalopathy (Wernicke)mentioning

confidence: 99%