Abstract
Alzheimer's disease is a devastating neurological disorder that affects more than 37 million people worldwide. The economic burden of Alzheimer's disease is massive; in the United States alone, the estimated direct and indirect annual cost of patient care is at least $100 billion. Current FDA-approved drugs for Alzheimer's disease do not prevent or reverse the disease, and provide only modest symptomatic benefits. Driven by the clear unmet medical need and a growing understanding of the molecular pathophysiology of Alzheimer's disease, the number of agents in development has increased dramatically in recent years. Truly *disease-modifying' therapies that target the underlying mechanisms of Alzheimer's disease have now reached late stages of human clinical trials. Primary targets include beta-amyloid, whose presence and accumulation in the brain is thought to contribute to the development of Alzheimer's disease, and tau protein which, when hyperphosphorylated, results in the self-assembly of tangles of paired helical filaments also believed to be involved in the pathogenesis of Alzheimer's disease. In this review, we briefly discuss the current status of Alzheimer's disease therapies under study, as well the scientific context in which they have been developed.
Highlights
Synaptotoxic β-amyloid (Aβ) peptide and the plaques composed of aggregated Aβ, as well as the neurofibrillary tangles composed of hyperphosphorylated tau protein, are believed to be central to the pathogenesis of Alzheimer's disease (AD)
Both the amyloid and tangle pathways present multiple opportunities to create disease-modifying therapies for AD, most of the biotech and pharmaceutical industry efforts have focused on the *amyloid hypothesis'; this focus is supported by strong genetic evidence implicating the primacy of the amyloid pathway [1]
Plaques are among the main strategies employed to slow the progression of AD
Summary
The anti-amyloid strategies are proceeding with the greatest number of candidate drugs. Numerous candidate disease-modifying therapies that target the underlying pathogenic mechanisms of AD are currently in clinical trials. While it is not possible to predict the success of any individual program, one or more are likely to prove effective. It seems reasonable to predict that in the nottoo-distant future, a synergistic combination of agents will have the capacity to alter the neurodegenerative cascade and reduce the global impact of this devastating disease
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