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Howard Feit, MD, PhD
Department of Neurology University of Texas Health Science Center at Dallas 5323 Harry Hines Blvd Dallas, TX 75235

Arch Neurol. 1983;40(8):528.

	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.

—Chromatin is the complex structure formed by the specific association of DNA with a variety of proteins, forming nucleosomes that in turn are arranged into a superhelix.¹ The biologic activity of chromatin as a template for transcription of DNA into RNA is directly related to its state of condensation.¹ Many degenerative diseases of the nervous system are associated with increased condensation of the chromatin, recognizable at the light microscopic level by the presence of shrunken, hyperchromatic nuclei. Bradley and Krasin² recently suggested the intriguing hypothesis that the chromatin alteration in the anterior horn cells of patients with amyotrophic lateral sclerosis (ALS) may be caused by lesions of the DNA that are not repaired.

Studies by Crapper et al³ and Lewis et al⁴ provided physical and biochemical evidence of an altered chromatin structure in Alzheimer's disease. Crapper et al³ first showed that . . . [Full Text PDF of this Article]

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