TY - JOUR
T1 - Brain reactive antibodies and the blood-brain barrier
T2 - observations in aging rodents and the effects of peripheral kainic acid
AU - Kulmala, Henrik K.
AU - Boja, John W.
AU - Albrecht, J. William
AU - Hutton, J. Thomas
N1 - Funding Information:
The hypothesis that the neurology of aging and AD may be caused by brain-reactive antibodies was raised several years ago [25]. Many investigators have demonstrated the presence of ‘Thisp roject was supported in part by a Biomedical Research Support Grant from NEOUCOM. The authors wish to acknowledge the expert assistance of Miss Y.S. Lynda Lee and Mr. Charles T. Kandiko. Thanks are also due to Drs. M.D. Schechter and B.K. Yamamoto for advice and assistance during the planning and conduct of this project. *From the Department of Pharmacology, Northeastern Ohio Universities, College of Medicine. Rootstown, Ohio 44272, U.S.A. ’From the Department of Medical Research Services, Veterans Administration Medical Center, Augusta, Georgia 30910, U.S.A. ‘From the Department of Medical and Surgical Neurology, Texas Tech University Health Sciences Center, Lubbock, Texas 79430, U.S.A.
Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1987
Y1 - 1987
N2 - This study was initiated to confirm the existence of brain-reactive autoantibodies and to determine if such antibodies have higher affinity for brain regions especially affected in Alzheimer’s disease. Serum collected from 90, 300, and 600 day old mice was incubated against brain tissues from these same mice, followed by incubation with fluorescently tagged rabbit antimouse IgG. No antibodies were present in the youngest serum, but considerable antibodies were present at 300 and, especially, at 600 days. Such antibodies were present in the blood vessels, but not in the brains of older animals. These antibodies, applied exogenously, labeled cells equally in all three ages of brains including most cortical and many other neurons, indicating that they are not neurotransmitter specific. In a further study, kainic acid or saline was administered peripherally to 15-month old rats. Kainic acid damaged the blood brain barrier and allowed the CNS entry of brain-reactive antibodies, especially into the subregions of hippocampus most damaged in Alzheimer’s.
AB - This study was initiated to confirm the existence of brain-reactive autoantibodies and to determine if such antibodies have higher affinity for brain regions especially affected in Alzheimer’s disease. Serum collected from 90, 300, and 600 day old mice was incubated against brain tissues from these same mice, followed by incubation with fluorescently tagged rabbit antimouse IgG. No antibodies were present in the youngest serum, but considerable antibodies were present at 300 and, especially, at 600 days. Such antibodies were present in the blood vessels, but not in the brains of older animals. These antibodies, applied exogenously, labeled cells equally in all three ages of brains including most cortical and many other neurons, indicating that they are not neurotransmitter specific. In a further study, kainic acid or saline was administered peripherally to 15-month old rats. Kainic acid damaged the blood brain barrier and allowed the CNS entry of brain-reactive antibodies, especially into the subregions of hippocampus most damaged in Alzheimer’s.
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U2 - 10.1080/03610738708259303
DO - 10.1080/03610738708259303
M3 - Article
C2 - 3678354
AN - SCOPUS:0023221525
VL - 13
SP - 67
EP - 72
JO - Experimental Aging Research
JF - Experimental Aging Research
SN - 0361-073X
IS - 2
ER -