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


     


This Article
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
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 Skias, D.
Right arrow Articles by Antel, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Skias, D.
Right arrow Articles by Antel, J. P.
NEUROLOGY 1985;35:1635
© 1985 American Academy of Neurology

Senile dementia of Alzheimer's type (SDAT)

Reduced T8+-cell-mediated suppressor activity

Demetrios Skias, Margaret Bania, Anthony T. Reder, Daniel Luchins and Jack P. Antel

From the Departments of Neurology (Drs. Skias, Bania, Reder, and Antel) and Psychiatry (Dr. Luchins) and the Brain Research Institute, The University of Chicago, Chicago, IL.

We compared patients with senile dementia of the Alzheimer's type (SDAT) and age-matched controls with respect to T8 -cell-mediated suppressor function using a pokeweed mitogen (pwm)-induced IgG secretion assay. The responding B cells were allogeneic to the T-regulator cells. T8-cell-mediated suppression was lower in SDAT patients than the controls when we used either 2 x 104 or 5 x 104 T8 cells. Suppressor function was lower in both SDAT and elderly controls than in young adults. SDAT patients and controls did not differ with regard to T4+ -cell-mediated helper activity. In SDAT patients, there seems to be an exaggeration of the age-related decline in suppressor-cell function. Whether such changes reflect accelerated changes of intrinsic lymphocyte properties or aberrant neural influences on lymphocytes remains to be resolved.

Address correspondence and reprint requests to Dr. Antel, Department of Neurology University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637.

Supported by grants from the Alzheimer Foundation and NIH AG01798.

Accepted for publication February 15, 1985.




This article has been cited by other articles:


Home page
Arch NeurolHome page
P. Bongioanni, B. Boccardi, M. Borgna, and B. Rossi
T-Lymphocyte Interleukin 6 Receptor Binding in Patients With Dementia of Alzheimer Type
Arch Neurol, October 1, 1998; 55(10): 1305 - 1308.
[Abstract] [Full Text] [PDF]


Home page
Arch NeurolHome page
P. Bongioanni, B. Boccardi, M. Borgna, M. Castagna, and C. Mondino
T-Cell Interferon Gamma Binding in Patients With Dementia of the Alzheimer Type
Arch Neurol, April 1, 1997; 54(4): 457 - 462.
[Abstract] [PDF]


Home page
LupusHome page
A. Juby, P. Davis, T. Genge, and J. McElhaney
Anticardiolipin antibodies in two elderly subpopulations
Lupus, December 1, 1995; 4(6): 482 - 485.
[Abstract] [PDF]


Home page
J Geriatr Psychiatry NeurolHome page
G. S. Zubenko
Endoplasmic Reticulum Abnormality in Alzheimer's Disease: Selective Alteration in Platelet NADH-Cytochrome C Reductase Activity
J Geriatr Psychiatry Neurol, January 1, 1989; 2(1): 3 - 10.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1985 by AAN Enterprises, Inc.