EFFECTS OF THE NOVEL IDO INHIBITOR DWG-1036 ON THE BEHAVIOUR AND NEUROCHEMISTRY OF THE TRIPLE TRANSGENIC MOUSE MODEL OF ALZHEIMER’S DISEASE
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Alzheimer’s disease (AD) is a neurodegenerative disorder causing memory loss as well as deficits in speech, motor performance and mood. Although the exact mechanisms causing the disease or how it progresses are not completely understood, amyloid beta 42 and tau are shown to be involved in neurodegeneration. In this thesis, we studied the role of the kynurenine pathway (KP) in the progression of behavioural and neurochemical deficits seen in AD. KP breaks down tryptophan, yet some of the by-products are known to be neurotoxic and involved in AD mechanisms, moreover KP is upregulated by amyloid beta 42. By inhibiting KP with a novel compound in the triple-transgenic mice and then testing them in a battery involving anxiety, cognition, motor and depression related tests, as well as studying their brains, for AD markers and KP metabolites using ELISA assays, we were able to further understand the role of KP in AD.