QUALITATIVE AND QUANTITATIVE DIFFERENCES IN SENILE PLAQUE DYSTROPHIC NEURITES OF ALZHEIMERS-DISEASE AND NORMAL AGED BRAIN

被引:61
作者
WANG, D
MUNOZ, DG
机构
[1] UNIV WESTERN ONTARIO,DEPT PATHOL,LONDON,ON N6A 5C1,CANADA
[2] ROBARTS RES INST,STROKE & AGING GRP,LONDON,ON,CANADA
关键词
ALZHEIMERS DISEASE; BETA-AMYLOID PROTEIN; BETA-AMYLOID PROTEIN PRECURSOR; CHROMOGRANIN A; TAU PROTEIN;
D O I
10.1097/00005072-199507000-00009
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
We have investigated the relationship of plaque dystrophic neurites expressing beta-amyloid precursor protein (beta APP) to those bearing markers of neurofibrillary degeneration (tau), or accumulating the synaptic protein chromogranin A (CgA). In cortical and hippocampal plaques in Alzheimer's disease (AD) beta APP colocalized with CgA in a neuritic population largely distinct from the subset of neurites labeled by tau. Putaminal plaques generally incorporated only CgA/beta APP, but not tan neurites, and with a rare exception cerebellar plaques were not associated with neurites. Neocortical and hippocampal plaques, the only common type in a group of elderly non-demented subjects (non-AD), incorporated CgA/beta APP, but not tau neurites. In addition to this qualitative difference between the two groups, neocortical plaques with CgA/beta APP neurites were one order of magnitude more common in AD than in non-AD. We propose a hierarchical model of plaque formation in which A beta deposits do not incorporate tau neurites unless neurites bearing synaptic proteins and beta APP are also present. Finally, the minimal association of tau neurites with putaminal plaques, in the presence of tau-immunoreactive neuropil threads and neurofibrillary tangles in the neighborhood, suggests that plaque-independent mechanisms of development of tau neurites operate in AD.
引用
收藏
页码:548 / 556
页数:9
相关论文
共 60 条
[1]   IMMUNOCHEMICAL IDENTIFICATION OF THE SERINE PROTEASE INHIBITOR ALPHA-1-ANTICHYMOTRYPSIN IN THE BRAIN AMYLOID DEPOSITS OF ALZHEIMERS-DISEASE [J].
ABRAHAM, CR ;
SELKOE, DJ ;
POTTER, H .
CELL, 1988, 52 (04) :487-501
[2]   DELAYED CHANGES OF CHROMOGRANIN-A IMMUNOREACTIVITY (CGA IR) IN HUMAN STRIATE CORTEX DURING POSTNATAL-DEVELOPMENT [J].
ANG, LC ;
GEORGE, DH ;
SHUL, D ;
WANG, DQ ;
MUNOZ, DG .
DEVELOPMENTAL BRAIN RESEARCH, 1992, 67 (02) :333-341
[3]   DEFINED NEUROFILAMENT, TAU-AMYLOID AND BETA-AMYLOID PRECURSOR PROTEIN EPITOPES DISTINGUISH ALZHEIMER FROM NON-ALZHEIMER SENILE PLAQUES [J].
ARAI, H ;
LEE, VMY ;
OTVOS, L ;
GREENBERG, BD ;
LOWERY, DE ;
SHARMA, SK ;
SCHMIDT, ML ;
TROJANOWSKI, JQ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (06) :2249-2253
[4]   ACCUMULATION OF ABNORMALLY PHOSPHORYLATED-TAU PRECEDES THE FORMATION OF NEUROFIBRILLARY TANGLES IN ALZHEIMERS-DISEASE [J].
BANCHER, C ;
BRUNNER, C ;
LASSMANN, H ;
BUDKA, H ;
JELLINGER, K ;
WICHE, G ;
SEITELBERGER, F ;
GRUNDKEIQBAL, I ;
IQBAL, K ;
WISNIEWSKI, HM .
BRAIN RESEARCH, 1989, 477 (1-2) :90-99
[5]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[6]   NEUROPIL THREADS OCCUR IN DENDRITES OF TANGLE-BEARING NERVE-CELLS [J].
BRAAK, H ;
BRAAK, E .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1988, 14 (01) :39-44
[7]  
CORIA F, 1988, LAB INVEST, V58, P454
[8]  
CORK LC, 1990, AM J PATHOL, V137, P1383
[9]   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
[10]  
CRAS P, 1990, AM J PATHOL, V137, P241