This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Robert J. Joynt, MD, PhD

JAMA. 1994;271(21):1686-1687.

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

Advances in molecular genetics marked the major advances last year in neurology; however, major developments also occurred in other areas, particularly in new types of therapy. Late last year, two excellent reviews summarizing advances in the genetics of neurologic diseases were published.^1,2 The unstable trinucleotide repeat continues to turn up as the genetic defect in several inherited neurologic disorders, including Huntington's disease, spinobulbar muscular atrophy, myotonic dystrophy, and spinocerebellar ataxia type 1.^1,2 The number of repeats is related to severity or latency in the different disorders.

Late-onset familial Alzheimer's disease (FAD) has been associated with a defect on chromosome 19.³ The defect is linked with apolipoprotein E, which transports cholesterol into the brain. Apolipoprotein E binds with amyloid and is found with amyloid and with the neurofibrillary tangles in the brain of those with Alzheimer's disease. The E4 allele of apolipoprotein E is found in 45% of . . . [Full Text PDF of this Article]

Author Affiliations
University of Rochester, Rochester, NY

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?