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Jay H. Robbins, MD
Dermatology Branch National Cancer Institute National Institutes of Health Bethesda, MD 20892

Arch Neurol. 1987;44(6):579-580.

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

To the Editor.

—In their SPECIAL ARTICLE, entitled "A New Hypothesis of the Etiology of Amyotrophic Lateral Sclerosis: The DNA Hypothesis," Bradley and Krasin¹ claimed that the hypothesis they presented was new. This claim is incorrect. The hypothesis that unrepaired DNA damage could be the cause of human neurodegenerative disease had previously been proposed by my colleagues and me in several publications._2-8 Although four^2,5,7,8 of these were cited in the Bradley and Krasin article, they were cited only for relatively unimportant information and not for the purpose of showing that they had previously set forth the hypothesis that Bradley and Krasin claimed as new and as their own.

The DNA-damage hypothesis proposed by my colleagues and me was based primarily on a decade of clinical and laboratory research on the disease xeroderma pigmentosum (XP).^2-7 We had specifically extended our hypothesis to neurodegenerations other than XP in . . . [Full Text PDF of this Article]

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