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Previous Volume 348:2489-2490 June 19, 2003 Number 25 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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The past 15 years, since the cloning of the gene for amyloid precursor protein, have witnessed breathtaking advances in our understanding of the pathophysiology of Alzheimer's disease, the most common cause of dementia. Most findings point to a final common pathway involving the accumulation in the brain of the toxic -amyloid peptide, a degradation product of amyloid precursor protein, resulting in progressive neuronal damage and concomitant cognitive deterioration. Notably, the border between Alzheimer's disease and vascular dementia has become increasingly blurred as shared pathologic processes have been identified.

Against this background comes the study by Verghese et al. in this . . . [Full Text of this Article]

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From the Department of Psychiatry, Harvard Medical School, Boston.

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