A role of autoimmune mechanisms in ichemic brain damage

被引:0
作者
Skvortsova, VI [1 ]
Sherstnev, VV
Gruden, MA
Myasoedov, NF
Stakhovskaya, LV
Efremova, NM
Hadzhieva, MK
Grivennikov, IA
Klyushnik, TP
Chaschikhina, EV
Kuzhilina, VB
机构
[1] Russian State Med Univ, Dept Neurol & Neurosurg, Moscow 117437, Russia
[2] PK Anokhin Normal Physiol Res Inst, Moscow, Russia
[3] Russian Acad Sci, Inst Mol Genet, Moscow 123182, Russia
[4] Russian Acad Med Sci, Ctr Mental Hlth, Moscow, Russia
来源
ZHURNAL NEVROPATOLOGII I PSIKHIATRII IMENI S S KORSAKOVA | 2001年
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中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The concentration of neurospecific proteins possessing neurotrophic properties (S100 beta and basic myelin protein - BMP), neurotrophine (nerve growth factor, NGF) and also titres of priumary and secondary antibodies in CSF and sera were measured in 25 patients with ischemic stroke in internal carotid territory and in sera of 40 patients with chronic cerebrovascular disease (cerebrovascular atherosclerosis and hypertonic encephalopathy). In stroke patients, several hours after onset, the titre of secondary antibodies to S100 beta and BMP was measured as elevated in serum (especially in atherotrombotic stroke) what witnesses for preformed sensibilization of brain tissue to neurospeciphic proteins. However, elevation of primary antibodies titre to NGF was registered only in CSF (they were normal in sera). NGF concentrations and secondary antibodies titre significantly correlated with stroke severity (correlation coefficients in relation to total clinical degree +0,42 and -0,78 respectively) what envisages grave prognostic importance. We revealed chronic autoimmunization to structural components of brain tissue in patients with chronic cerebrovascular disease). The ratio of primary/secondary antibodies to S100 beta and BMP titres reflects the acuteness of antibody formation as and may support the suggestion about changes in blood-brain barrier (BBB) permeability. We failed to reveal sensibilization to NGF in chronic cerebrovascular disease what may explain that there was no neurological deficit in these patients. Neuroprotective therapy with glycine (600 mg/day) administered to patients with chronic cerebrovascular disease, appeared to improve clinincal status and antibody concentration in sera. We suppose that such a therapy may be beneficial as preventive.
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页码:46 / 54
页数:9
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共 43 条
[1]  
[Anonymous], 1985, Stroke, V16, P885
[2]  
AURELL A, 1987, STROKE, V18, P911
[3]   Serum S-100 protein in acute stroke [J].
Butterworth, RJ ;
Sherwood, RA ;
Bath, PMW .
STROKE, 1998, 29 (03) :730-730
[4]  
CHEKHONIN VP, 1995, MONOKLONALNYE ANTITE, P160
[5]  
Chen SC, 1996, ADV NEUROL, V71, P433
[6]   THYMOCYTE APOPTOSIS INDUCED BY P53-DEPENDENT AND INDEPENDENT PATHWAYS [J].
CLARKE, AR ;
PURDIE, CA ;
HARRISON, DJ ;
MORRIS, RG ;
BIRD, CC ;
HOOPER, ML ;
WYLLIE, AH .
NATURE, 1993, 362 (6423) :849-852
[7]   ROLE OF NEUROTROPHIC FACTORS IN DEVELOPMENT [J].
DAVIES, AM .
TRENDS IN GENETICS, 1988, 4 (05) :139-143
[8]   TEMPORAL ANALYSIS OF EVENTS ASSOCIATED WITH PROGRAMMED CELL-DEATH (APOPTOSIS) OF SYMPATHETIC NEURONS DEPRIVED OF NERVE GROWTH-FACTOR [J].
DECKWERTH, TL ;
JOHNSON, EM .
JOURNAL OF CELL BIOLOGY, 1993, 123 (05) :1207-1222
[9]   Proinflammatory cytokines: Indicators of infection in high-risk patients [J].
Fassbender, K ;
Dempfle, CE ;
Mielke, O ;
Rossol, S ;
Schneider, S ;
Dollman, M ;
Hennerici, M .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1997, 130 (05) :535-539
[10]   ANALYSIS OF CELL CYCLE-RELATED GENE-EXPRESSION IN POSTMITOTIC NEURONS - SELECTIVE INDUCTION OF CYCLIN D1 DURING PROGRAMMED CELL-DEATH [J].
FREEMAN, RS ;
ESTUS, S ;
JOHNSON, EM .
NEURON, 1994, 12 (02) :343-355