Thiamine Deficiency as a Model of Selective Neurodegeneration with Chronic Oxidative Deficits
Part of the
GWUMC Department of Biochemistry and Molecular Biology Annual Spring Symposia
book series (GWUN)
Experimental thiamine deficiency is a classical model of the molecular changes that underlie the clinical syndrome referred to variously as delirium, acute confusional state1,2,3,4 or metabolic encephalopathy5. This syndrome is characterized by decreased attention and cognition, alertness, orientation and grasp, memory, affect and perception. A wide variety of systemic disorders lead to the development of the syndrome including hypoxia, ischemia, hypoglycemia, some diseases of peripheral organs, ionic imbalance, poisoning, dysfunction of temperature regulation, infection or inflammation of the brain and spinal cord, primary neuronal and glial disorders, acute delirious states (sedative drug withdrawal, drug intoxication, postoperative delirium, intensive care unit delirium), and vitamin and nutritional deficiencies (e.g. thiamine deficiency). Despite the varied etiology, the diverse insults that lead to delirium may act by common metabolic and cellular pathways, as suggested by results from studies of aging and hypoxia.6,7,8
KeywordsAmyloid Precursor Protein Inferior Colliculus Thiamine Deficiency Medial Geniculate Nucleus Intensive Care Unit Delirium
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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