THE IMMUNOPATHOLOGY OF ALZHEIMERS-DISEASE AND SOME RELATED DISORDERS

被引:73
作者
KALARIA, RN
机构
[1] CASE WESTERN RESERVE UNIV, SCH MED, DEPT NEUROL, CLEVELAND, OH 44106 USA
[2] CASE WESTERN RESERVE UNIV, SCH MED, CLEVELAND, OH 44106 USA
关键词
D O I
10.1111/j.1750-3639.1993.tb00761.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Current evidence clearly indicates that elements of the immune system are involved in the pathogenesis of the principal lesions characterizing Alzheimer's disease (AD). Findings are in accord with features associated with both the innate and adaptive immune mechanisms involved in a predominantly local inflammatory response within the parenchyma. Many of the features are unique to AD, presumably related to the unusual properties of beta amyloid protein. Remarkably, the brain holds the capacity to produce almost all the immune system mediators which largely seem to be generated by glia comprising both astrocytes and microglia. While a variety of humoral mediators including classical acute phase proteins (and serpins) are increased and released, the complement seems most intrinsically involved. The cellular response is elaborated by microglia which seem the main immunocompetent cells partaking in the response. These appear to function as pluripotent macrophages expressing both classes of MHC antigens. Further characterization of this interesting response to cerebral amyloidosis will be challenging.
引用
收藏
页码:333 / 347
页数:15
相关论文
共 138 条
[121]   THE MOLECULAR PATHOLOGY OF ALZHEIMERS-DISEASE [J].
SELKOE, DJ .
NEURON, 1991, 6 (04) :487-498
[122]   DETECTION OF BRAIN AUTOANTIBODIES IN THE SERUM OF PATIENTS WITH ALZHEIMERS-DISEASE BUT NOT DOWNS-SYNDROME [J].
SINGH, VK ;
FUDENBERG, HH .
IMMUNOLOGY LETTERS, 1986, 12 (5-6) :277-280
[123]   SENILE DEMENTIA OF ALZHEIMERS TYPE (SDAT) - REDUCED T8+-CELL-MEDIATED SUPPRESSOR ACTIVITY [J].
SKIAS, D ;
BANIA, M ;
REDER, AT ;
LUCHINS, D ;
ANTEL, JP .
NEUROLOGY, 1985, 35 (11) :1635-1638
[124]   ADHESION RECEPTORS OF THE IMMUNE-SYSTEM [J].
SPRINGER, TA .
NATURE, 1990, 346 (6283) :425-434
[125]   GENETIC-LINKAGE STUDIES SUGGEST THAT ALZHEIMERS-DISEASE IS NOT A SINGLE HOMOGENEOUS DISORDER [J].
STGEORGEHYSLOP, PH ;
HAINES, JL ;
FARRER, LA ;
POLINSKY, R ;
VAN BROECKHOVEN, C ;
GOATE, A ;
MCLACHLAN, DRC ;
ORR, H ;
BRUNI, AC ;
SORBI, S ;
RAINERO, I ;
FONCIN, JF ;
POLLEN, D ;
CANTU, JM ;
TUPLER, R ;
VOSKRESENSKAYA, N ;
MAYEUX, R ;
GROWDON, J ;
FRIED, VA ;
MYERS, RH ;
NEE, L ;
BACKHOVENS, H ;
MARTIN, JJ ;
ROSSOR, M ;
OWEN, MJ ;
MULLAN, M ;
PERCY, ME ;
KARLINSKY, H ;
RICH, S ;
HESTON, L ;
MONTESI, M ;
MORTILLA, M ;
NACMIAS, N ;
GUSELLA, JF ;
HARDY, JA .
NATURE, 1990, 347 (6289) :194-197
[126]  
STRAUSS S, 1992, LAB INVEST, V66, P223
[127]   EPIDERMAL GROWTH-FACTOR RECEPTOR EXPRESSION IN DEMENTED AND AGED HUMAN BRAIN [J].
STYREN, SD ;
MUFSON, EJ ;
STYREN, GC ;
CIVIN, WH ;
ROGERS, J .
BRAIN RESEARCH, 1990, 512 (02) :347-352
[128]   IMMUNOLOGICAL INDEXES IN PRESENILE ALZHEIMERS-DISEASE [J].
TAVOLATO, B ;
ARGENTIERO, V .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1980, 46 (03) :325-331
[129]  
TOMLINSON BE, 1992, GREENFIELDS NEUROPAT, P1141
[130]   IMMUNOHISTOCHEMICAL STUDY OF ALPHA-2 MACROGLOBULIN RECEPTOR IN ALZHEIMER AND CONTROL POSTMORTEM HUMAN BRAIN [J].
TOOYAMA, I ;
KAWAMATA, T ;
AKIYAMA, H ;
MOESTRUP, SK ;
GLIEMANN, J ;
MCGEER, PL .
MOLECULAR AND CHEMICAL NEUROPATHOLOGY, 1993, 18 (1-2) :153-160