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Previous Volume 357:933-935 August 30, 2007 Number 9 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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During the next few decades, millions of baby boomers will enter their 70s, 80s, and 90s, quadrupling the number of patients with Alzheimer's disease, the leading cause of dementia in the elderly. Despite remarkable advances in the past 20 years in our understanding of the molecular genetics and biology of Alzheimer's disease, no therapeutic advances have altered this troubling statistic. A recent and unexpected study by Roberson and colleagues¹ is therefore especially welcome.

The authors had previously developed mice expressing a variant of human amyloid precursor protein encoded by a gene carrying two mutations linked to early-onset familial Alzheimer's disease.² . . . [Full Text of this Article]

Source Information

From the Department of Neurology, University of Minnesota Medical School, Minneapolis.

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