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Background
Alzheimer’s disease (AD) affects one in every nine adults age 65 and older and is the sixth leading cause of death in the United States. As the average life expectancy increases, the incidence of AD is expected to increase dramatically. By 2025, the number of individuals 65 years of age and older with AD is expected to reach 7.1 million, while this number is projected to reach 13.8 million people by 2050. If the current trend continues, healthcare, long-term care, and hospice care are projected to increase from a current mark of $203 billion to $1.2 trillion in 2050. Meanwhile, pharmacologic treatments for AD have ineffective at slowing or halting the disease. Therefore, it is imperative that alternative therapeutic targets be explored.
AD is characterized by extracellular plaques composed of beta-amyloid (Aβ), neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau, and neuron loss. We primarily examine alterations in tau, at time points before neuronal loss is observed. To do so, we use multiple rodent models.