Over-activation of the KP has been implicated in the pathogenesis of several neurological disorders including Huntington’s disease (HD), Alzheimer’s disease (AD), and the acquired immunodeficiency syndrome (AIDS)-dementia complex.13–17 The pathway is regulated by the immune-factor responsive enzyme indoleamine-2,3-dioxygenase (IDO) in most cells and by tryptophan-2,3 dioxygenase (TDO) in the liver which is modulated by tryptophan and glucocorticoids.18,19. This evidence concerns the gene TDO2 and early-onset autosomal dominant Alzheimer disease.