Abstract
Alzheimer’s disease (AD) currently affects 44 million people worldwide, yet there are no effective treatments to cure or prevent this devastating disease. Two major hallmarks of the AD brain are extracellular plaques, containing various forms of amyloid-β protein (Aβ), and intracellular neurofibrillary tangles, composed of hyperphosphorylated tau protein. Active and passive vaccines against various forms of Aβ have shown promise in preclinical animal models; however, translating these results safely and effectively into humans has been challenging. Over the past decade, these vaccines have shown some target engagement but little or no cognitive efficacy, possibly due to late intervention in patients who have had AD symptoms for years. Many clinical trials are now under way to treat individuals at risk for AD prior to or in the earliest stages of cognitive decline with the hope of preventing or delaying the onset of the disease. Early results look promising.
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