NEUROIMMUNE MECHANISMS IN ALZHEIMER-DISEASE PATHOGENESIS

被引：157

作者：

MCGEER, PL ^{[1
]}

ROGERS, J ^{[1
]}

MCGEER, EG ^{[1
]}

机构：

[1] SUN HLTH RES INST,SUN CITY,AZ

来源：

ALZHEIMER DISEASE & ASSOCIATED DISORDERS | 1994年 / 8卷 / 03期

关键词：

NEUROIMMUNE MECHANISMS; BETA-AMYLOID PROTEIN; GLYCOPROTEINS; MEMBRANE ATTACK COMPLEX; COMPLEMENT; T CELLS;

D O I：

10.1097/00002093-199408030-00001

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Lesions in Alzheimer disease are characterized by the assembly of a variety of cells and proteins associated with the immune system. Activated microglia express high levels of major histocompatibility complex glycoproteins and receptors for complement. Small numbers of T lymphocytes infiltrate tissue. Proteins of the classical complement pathway are closely connected with beta-amyloid deposits. beta-Amyloid protein binds C1q in vitro and activates the pathway. The membrane attack complex of complement, as well as proteins that defend against that complex, colocalize with dystrophic neurites. These data imply that an autodestructive process is occurring in Alzheimer disease, that overactive microglia might be responsible, and that antiinflammatory drugs might be an effective form of therapy.

引用

页码：149 / 158

页数：10

共 60 条

[1] ASSOCIATION OF AMYLOID-P COMPONENT WITH COMPLEMENT PROTEINS IN NEUROLOGICALLY DISEASED BRAIN-TISSUE [J].