DIFFERENTIAL EXPRESSION OF TGF-BETA-1, TGF-BETA-2 AND TGF-BETA-3 ISOTYPES IN ALZHEIMERS-DISEASE - A COMPARATIVE IMMUNOHISTOCHEMICAL STUDY WITH CEREBRAL INFARCTION, AGED HUMAN AND MOUSE CONTROL BRAINS

被引:89
作者
PERESS, NS
PERILLO, E
机构
[1] DEPT VET AFFAIRS MED CTR,PATHOL SERV,NORTHPORT,NY
[2] DEPT VET AFFAIRS MED CTR,RES SERV,NORTHPORT,NY
关键词
ALZHEIMERS DISEASE; ASTROCYTES; CEREBRAL INFARCTION; CYTOKINES; MICROGLIA; TGF-BETA;
D O I
10.1097/00005072-199511000-00007
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Based upon the hypothesis that growth regulatory and inflammatory mechanisms participate in the pathogenesis of Alzheimer's disease, we studied cases of Alzheimer's disease for immunoreactivity to each of the three mammalian transforming growth factor beta (TGF-beta) isotypes: TGF-beta 1, TGF-beta 2, TGF-beta 3. Results were compared with those seen in control brains and in a destructive pathological process, subacute infarction. In the cases of Alzheimer's disease, TGF-beta 1 immunoreactivity was limited to neuritic profiles within senile plaques. Neuronal neurofibrillary tangles, plaque neurites, microglia, astrocytes and macrophages expressed TGF-beta 2 immunoreactivity. TGF-beta 3 produced strikingly selective staining of Hirano bodies. In contrast, in cases with infarction, reactive astrocytes and macrophages were positive with all three antibodies. Ramified microglia labeled selectively, as in the Alzheimer brains, with the TGF-beta 2 antibody. Subtle generalized astrocyte and microglial immunoreactivity for TGF-beta 2 was seen in pathological and control brains. The localization of TGF-beta isotypes to the lesions of Alzheimer's disease supports the hypothesis that these cytokines may influence lesion expression. Their presence in reactive cells associated with cerebral infarction suggest that they may play a broader role in the pathogenesis of CNS disease.
引用
收藏
页码:802 / 811
页数:10
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