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 12days 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 12days 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.