β-AMYLOID AS A MOLECULAR THERAPEUTIC TARGET IN ALZHEIMER'S DISEASE

Alzheimer's disease is the most common form of dementia, primarily affecting individuals during or after their sixth decade of life. Despite decades of research, there are still no effective disease-modifying drugs available to treat this neurodegenerative disorder. Current FDA-approved medications primarily offer symptomatic relief and are based upon known neurotransmitter deficits. There are, however, many drugs in preclinical and clinical development which target other aspects of AD pathogenesis. Principal among these are drugs which modulate beta-amyloid, a protein that is believed to be central to the cascade which leads to the development of Alzheimer's disease. This article will outline the metabolism of P-amyloid and review a number of different strategies, including pitfalls and future directions of such methods that are directed towards the modulation of this protein. It will become clear that beta-amyloid represents a potent molecular target for pharmacological manipulation to perhaps prevent the onset and progression of Alzheimer's disease.