SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
Journal of Geriatric Psychiatry and Neurology
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Ringman, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ringman, J. M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

What the Study of Persons At Risk for Familial Alzheimer's Disease Can Tell Us About the Earliest Stages of the Disorder: A Review

John M. Ringman, MD

UCLA Alzheimer Disease Center, Los Angeles, CA, jringman{at}mednet.ucla.edu

As the proportion of elderly persons continues to expand, understanding the pathobiology of Alzheimer's disease and being able to diagnose it at an early stage become more critical. A minority of Alzheimer's disease cases are inherited as a fully-penetrant, autosomal dominant trait with a young age of onset. The molecular study of the pathogenic mutations has led to insights regarding the etiology of sporadic Alzheimer's disease. Clinical studies in persons at risk for these mutations have confirmed early episodic memory and executive deficits in Alzheimer's disease and suggested that dysphoria may precede the cognitive changes of Alzheimer's disease. Imaging studies have indicated that medial temporal lobe atrophy begins 3 to 4 years before cognitive symptoms, and quantitative cerebral metabolic changes are also present from early on. Studies of biochemical markers suggest that elevations of plasma A 1-42 occur early in familial Alzheimer's disease but that tau may not be elevated in cerebrospinal fluid until the disease is more advanced.

Key Words: presenilin-1 • amyloid precursor protein • Alzheimer's disease • genetic risk • familial • preclinical • presymptomatic • neuroimaging • biomarkers • cognitive • behavioral • neuropsychology

Journal of Geriatric Psychiatry and Neurology, Vol. 18, No. 4, 228-233 (2005)
DOI: 10.1177/0891988705281878


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    What's this?


This article has been cited by other articles:


Home page
BrainHome page
J. R. Hodges
Alzheimer's centennial legacy: origins, landmarks and the current status of knowledge concerning cognitive aspects.
Brain, November 1, 2006; 129(Pt 11): 2811 - 2822.
[Abstract] [Full Text] [PDF]


Home page
J Geriatr Psychiatry NeurolHome page
L. F. Jarvik and D. Blazer
Children of Alzheimer Patients: An Overview
J Geriatr Psychiatry Neurol, December 1, 2005; 18(4): 181 - 186.
[PDF]



Advertisement