PDGF IS ASSOCIATED WITH NEURONAL AND GLIAL ALTERATIONS OF ALZHEIMERS-DISEASE

被引:35
作者
MASLIAH, E
MALLORY, M
ALFORD, M
DETERESA, R
SAITOH, T
机构
[1] University of California., San Diego, School of Medicine, Department of Neurosciences, La Jolla
关键词
PLATELET-DERIVED GROWTH FACTOR; ALZHEIMERS DISEASE; NEUROFIBRILLARY TANGLES; NEURITIC PLAQUES; SPROUTING;
D O I
10.1016/0197-4580(95)00050-O
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
In the present study we observed that while platelet-derived growth factor (PDGF)-BB is exclusively expressed by neurons in the human brain, PDGF-AA is expressed in neurons and blood vessels. In Alzheimer's disease (AD), antibodies against PDGF-BB (but not PDGF-AA) recognized the neurofibrillary alterations of this disease. The levels of PDGF-BB correlated with the patterns of synaptic loss and sprouting while PDGF-AA immunostaining of the vessels was correlated with glial proliferation. Immunostaining was completely abolished when the antibodies were preincubated with their respective purified recombinant PDGF. Western blot analysis showed that antibodies against PDGF recognized a 31 kDa protein that was mildly increased in AD. These data suggest that PDGF, as well as other neurotrophic factors, play an important role in the mechanisms of neurofibrillary pathology in AD.
引用
收藏
页码:549 / 556
页数:8
相关论文
共 49 条
[1]  
BARCIKOWSKA M, 1992, NEUROPATHOLOGIA POLS, P227
[2]   CASEIN KINASE-II IS ASSOCIATED WITH NEUROFIBRILLARY TANGLES BUT IS NOT AN INTRINSIC COMPONENT OF PAIRED HELICAL FILAMENTS [J].
BAUM, L ;
MASLIAH, E ;
IIMOTO, DS ;
HANSEN, LA ;
HALLIDAY, WC ;
SAITOH, T .
BRAIN RESEARCH, 1992, 573 (01) :126-132
[3]   EVIDENCE FOR AXONAL LOSS IN REGIONS OCCUPIED BY SENILE PLAQUES IN ALZHEIMER CORTEX [J].
BENES, FM ;
FAROL, PA ;
MAJOCHA, RE ;
MAROTTA, CA ;
BIRD, ED .
NEUROSCIENCE, 1991, 42 (03) :651-660
[4]   IMMUNOREACTIVE EPIDERMAL GROWTH-FACTOR RECEPTORS IN NEURITIC PLAQUES FROM PATIENTS WITH ALZHEIMERS-DISEASE [J].
BIRECREE, E ;
WHETSELL, WO ;
STOSCHECK, C ;
KING, LE ;
NANNEY, LB .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1988, 47 (05) :549-560
[5]  
COTMAN CW, 1989, RES PER ALZ, P54
[6]   SENILE PLAQUE NEURITES IN ALZHEIMER-DISEASE ACCUMULATE AMYLOID PRECURSOR PROTEIN [J].
CRAS, P ;
KAWAI, M ;
LOWERY, D ;
GONZALEZDEWHITT, P ;
GREENBERG, B ;
PERRY, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (17) :7552-7556
[7]   A QUANTITATIVE MORPHOMETRIC ANALYSIS OF THE NEURONAL AND SYNAPTIC CONTENT OF THE FRONTAL AND TEMPORAL CORTEX IN PATIENTS WITH ALZHEIMERS-DISEASE [J].
DAVIES, CA ;
MANN, DMA ;
SUMPTER, PQ ;
YATES, PO .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1987, 78 (02) :151-164
[8]   SYNAPSE LOSS IN FRONTAL-CORTEX BIOPSIES IN ALZHEIMERS-DISEASE - CORRELATION WITH COGNITIVE SEVERITY [J].
DEKOSKY, ST ;
SCHEFF, SW .
ANNALS OF NEUROLOGY, 1990, 27 (05) :457-464
[9]   NEUROPATHOLOGICAL CHANGES IN SCRAPIE AND ALZHEIMERS-DISEASE ARE ASSOCIATED WITH INCREASED EXPRESSION OF APOLIPOPROTEIN-E AND CATHEPSIN-D IN ASTROCYTES [J].
DIEDRICH, JF ;
MINNIGAN, H ;
CARP, RI ;
WHITAKER, JN ;
RACE, R ;
FREY, W ;
HAASE, AT .
JOURNAL OF VIROLOGY, 1991, 65 (09) :4759-4768
[10]   SENILE PLAQUES AS ABERRANT SPROUT-STIMULATING STRUCTURES [J].
GEDDES, JW ;
ANDERSON, KJ ;
COTMAN, CW .
EXPERIMENTAL NEUROLOGY, 1986, 94 (03) :767-776