You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 61 No. 3, March 2004 TABLE OF CONTENTS
  Archives
  •  Online Features
  Editorial
 This Article
 •Full text
 •PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citing articles on Web of Science (1)
 •Contact me when this article is cited
 Related Content
 •Related article
 •Similar articles in this journal
 Topic Collections
 •Amyotrophic Lateral Sclerosis
 •Dementias
 •Neurogenetics
 •Neuromuscular diseases
 •Alert me on articles by topic
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

A Frontotemporal Family Bridge

Arch Neurol. 2004;61:318.

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

One of the major discoveries in dementia has been the linkage of a family with disinhibition-dementia-parkinsonism amyotrophy complex to chromosome 17.1 Soon after that, several other families were linked to chromosome 17, many described before, under various names, such as hereditary dysphasic dementia2 and pallido-ponto-nigral degeneration.3 It was soon recognized that all these conditions have clinical and pathological resemblance to sporadic frontotemporal dementia (FTD), primary progressive aphasia, and corticobasal ganglionic degeneration (CBD). A conference about chromosome 17–linked dementias agreed on the apt term frontotemporal dementia with parkinsonism linked to chromosome 17.4 Although Wilhelmsen considered tau the candidate gene, tau mutations were described later.5-6

Not all dementias linked to chromosome 17 have tau mutations; probably only about 50% do. Approximately 25% to 40% of FTD is familial, and approximately 10% to 30% of patients with a positive family history have a mutation in tau.7 None of the sporadic . . . [Full Text of this Article]

Andrew Kertesz, MD, FRCPC
Department of Clinical Neurological Sciences
St. Joseph's Hospital
268 Grosvenor St
London, Ontario
Canada N6A 4V2
(e-mail: andrew.kertesz@sjhc.london.on.ca)



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

RELATED ARTICLE

17q-Linked Frontotemporal Dementia–Amyotrophic Lateral Sclerosis Without Tau Mutations With Tau and {alpha}-Synuclein Inclusions
Kirk C. Wilhelmsen, Mark S. Forman, Howard J. Rosen, Loren I. Alving, Jill Goldman, Jennie Feiger, James V. Lee, Samantha K. Segall, Joel H. Kramer, Catherine Lomen-Hoerth, Katherine P. Rankin, Julene Johnson, Heidi S. Feiler, Michael W. Weiner, Virginia M.-Y. Lee, John Q. Trojanowski, and Bruce L. Miller
Arch Neurol. 2004;61(3):398-406.
ABSTRACT | FULL TEXT  






HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2004 American Medical Association. All Rights Reserved.