Thiamine deficiency is known to increase the expression of BACE-1, activate the glial fibrillary acidic protein, decrease the activity of the alpha-ketoglutarate dehydrogenase complex, and trigger the production of proinflammatory cytokines such as TNF-α in AD mice, leading to the accumulation of Aβ plaques [83]. The gene discussed is BACE1; the disease is Alzheimer disease.