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Alzheimer’s Disease (AD) affects at least 5.7 million Americans, and it is the sixth leading cause of death in the United States. At the onset, patients experience minor memory problems. Next, impairments in speech and motor function manifest as a limitation to well-being and independence. Slowing this pandemic rise is critical, since AD also bears a huge socioeconomical burden. Unfortunately, there is limited prevention and no effective cure has been found, as all clinical trials for promising AD drugs have failed thus far. The pathological hallmarks of AD include amyloid-β plaques (Aβ), neurofibrillary tangles (NFT), and neuroinflammation. Other factors include APOE4 and environmental stressors, such as metal dyshomeostasis, which contribute to AD pathogenesis. Herein, we review major contributing factors involved in AD pathophysiology. Deeper understanding of associated molecular mechanisms underlying AD pathogenesis is critical for developing novel AD theranostics.
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