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The classical neuropathologic features of Alzheimer disease (AD) are extracellular amyloid plaque deposition and intracellular neurofibrillary tangle formation, associated with neuronal and synaptic loss and reactive gliosis. Multiple processes are implicated in the initiation and propagation of the pathologic changes in the AD brain—the primary focus being on amyloid precursor protein and amyloid β-protein (Aβ) metabolism, and tau phosphorylation and polymerization. Nonetheless, the causes of neuronal death in stereotypical anatomic regions in AD brain are uncertain. The article by Yao et al. in this issue of Neurology supports oxidative stress as a mechanism of neuronal toxicity in AD, a process amenable to therapeutic intervention.1
Oxidative stress refers to the balance between the generation of highly reactive oxygen species and the antioxidant defenses that clear these molecules. Normal neuronal function relies on a high level …
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