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Alzheimer's disease (AD) is not a simple disorder, meaning that its pathology affects many brain areas and neuronal functions on all levels. It is known that patients with this neurodegenerative disease show significant changes in 1) brain energy metabolism (more specifically, in how the brain uses glucose, the primary brain fuel) leading to energy shortage; 2) changes in insulin signalling in the brain, potentially leading to disruptions in many functions such as memory formation/maintenance; and 3) oxidative stress levels. Simple, single-target AD treatment attempts have all failed up to now. We suggest that due to the complexity of AD, any effective treatment should target all of the major pathways of AD changes. We show that chronic treatment designed to improve energy state of the brain, reduce oxidative stress and restore insulin signalling, leads to a complete prevention of Alzheimer's progression in mouse models of the disease.

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This page is a summary of: Triple-target treatment for Alzheimer’s: Correcting hypometabolism, oxidative stress, and neuroinflammation, Alzheimer s & Dementia, July 2015, Elsevier,
DOI: 10.1016/j.jalz.2015.07.211.
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