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Dilemmas and Directions

Arch Neurol. 1999;56:1441-1442.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

IN THIS issue, Sabbagh et al¹ attempt to shed light on the pathophysiology of the Lewy body variant of Alzheimer disease (LBV). This is another important step in a long journey. The association of Lewy bodies with Parkinson disease was made in 1912; the first report of Lewy bodies in association with dementia, in 1961.² Since then, owing to the development of immunostaining techniques for the Lewy body–associated protein ubiquitin, and more recently for I-synuclein, an increasingly strong link has been established between the presence of extranigral Lewy bodies and the development of dementing illness in which extrapyramidal symptoms may follow the onset of dementia or may not occur at all. In fact, late-life dementia associated with Lewy bodies is probably second in prevalence only to Alzheimer disease (AD), occurring in approximately 20% of persons diagnosed while alive with probable AD.³ Is this the coincidence of 2 diseases (after all, . . . [Full Text of this Article]

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