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Alzheimer disease (AD) is a devastating neurodegenerative disorder that eventually results in dementia. Currently, there are no disease-modifying therapies for AD and the few available symptomatic treatments are of limited benefit. Thus, there is a pressing need to better understand this disease in order to develop effective treatments and to detect the disease in individuals before they exhibit extensive brain atrophy. This article series examines our current understanding of the pathophysiology of AD and some of the approaches being used to study this disease.
Oxidative damage plays a key role in the development of Alzheimer disease. In this Review, Butterfield and Halliwell discuss how this damage relates to impaired brain glucose metabolism and proteostasis defects and how knowledge of it may suggest potential therapies.
Understanding the complex interplay of cells that protect neurons early in Alzheimer disease but later contribute to neurodegeneration is important for developing effective therapeutics. In this Review, Henstridge and colleagues discuss the contributions of multiple cell types to disease pathogenesis.
Various techniques can be used to image aspects of the pathophysiology of Alzheimer disease in humans, notably protein deposition and neurodegeneration. In this Review, William Jagust discusses how human neuroimaging studies have shaped our understanding of this disease.
Rodent models are extensively used to investigate the pathophysiology of Alzheimer disease. In this Review, Götz, Bodea and Goedert critically examine the approaches that have been adopted to generate rodent Alzheimer disease models and touch on some of the lessons that have been learned from their use.