Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lacomblez, L.
Right arrow Articles by Meininger, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lacomblez, L.
Right arrow Articles by Meininger, V.
Related Collections
Right arrow Amyotrophic lateral sclerosis
Right arrow All epidemiology
Neurology 2002;58:1112-1114
© 2002 American Academy of Neurology


Brief Communications

APOE: A potential marker of disease progression in ALS

L. Lacomblez, MD, V. Doppler, MD, I. Beucler, PhD, G. Costes, F. Salachas, MD, A. Raisonnier, MD, N. Le Forestier, MD, P.-F. Pradat, MD, E. Bruckert, MD and V. Meininger, MD

From the Fédération de Neurologie Mazarin (Drs. Lacomblez, Doppler, Salachas, Le Forestier, Pradat, and Meininger), Service de Pharmacologie (Drs. Lacomblez and Doppler), Service d’Endocrinologie (Dr. Bruckert), and Laboratoire des Lipides et Lipoprotéines (Drs. Beucler and Raisonnier, and G. Costes), AP-HP, Hôpital de la Salpêtrière, Paris, France.

Address correspondence and reprint requests to Dr. Vincent Meininger, Hôpital de la Salpêtrière, 47 boulevard de l’Hôpital, 75013 Paris, France; e-mail: vincent.meininger{at}psl.ap-hop-paris.fr

Although documented in AD, the role of APOE remains unclear in ALS. APOE phenotype and plasma levels were measured in 403 patients with ALS and were correlated with clinical parameters and survival time. No correlations were observed between the APOE phenotype and these variables. In contrast, APOE plasma levels were correlated with both rate of deterioration and survival time and appeared to be an important risk factor for decreased survival time with a relative risk of 0.647 (95% CI: 0.465 to 0.901; p = 0.01).




This article has been cited by other articles:


Home page
J. Neurosci.Home page
Q. Xu, D. Walker, A. Bernardo, J. Brodbeck, M. E. Balestra, and Y. Huang
Intron-3 Retention/Splicing Controls Neuronal Expression of Apolipoprotein E in the CNS
J. Neurosci., February 6, 2008; 28(6): 1452 - 1459.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
R. W. Mahley, K. H. Weisgraber, and Y. Huang
Inaugural Article: Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, including Alzheimer's disease
PNAS, April 11, 2006; 103(15): 5644 - 5651.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
Z.-S. Ji, K. Mullendorff, I. H. Cheng, R. D. Miranda, Y. Huang, and R. W. Mahley
Reactivity of Apolipoprotein E4 and Amyloid beta Peptide: LYSOSOMAL STABILITY AND NEURODEGENERATION
J. Biol. Chem., February 3, 2006; 281(5): 2683 - 2692.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
F. M. Harris, W. J. Brecht, Q. Xu, I. Tesseur, L. Kekonius, T. Wyss-Coray, J. D. Fish, E. Masliah, P. C. Hopkins, K. Scearce-Levie, et al.
Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic mice
PNAS, September 16, 2003; 100(19): 10966 - 10971.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2002 by AAN Enterprises, Inc.