Elevated connexin43 immunoreactivity at sites of amyloid plaques in Alzheimer's disease

被引:155
作者
Nagy, JI
Li, W
Hertzberg, EL
Marotta, CA
机构
[1] ALBERT EINSTEIN COLL MED,DEPT NEUROSCI,BRONX,NY 10461
[2] ALBERT EINSTEIN COLL MED,DEPT ANAT & STRUCT BIOL,BRONX,NY 10461
[3] BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912
[4] BROWN UNIV,DEPT NEUROSCI,PROVIDENCE,RI 02912
[5] MIRIAM HOSP,PROVIDENCE,RI 02906
关键词
connexin43; gap junction; astrocyte; beta/A4; amyloid; Alzheimer's disease;
D O I
10.1016/0006-8993(95)01526-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The distribution of the astrocytic gap junctional protein, connexin43 (Cx43) was compared immunohistochemically with that of amyloid plaques in Alzheimer's Disease (AD) brain. By light microscopy, cortical areas containing numerous beta/A4 amyloid plaques exhibited increased immunostaining density for Cx43 and some plaques corresponded exactly to sites of intensified Cx43 immunoreactivity. By electron microscopy, Cx43 was localized to astrocytic gap junctions in AD brain. Increased Cx43 expression in AD may represent an attempt to maintain tissue homeostasis by augmented intercellular communication via gap junction formation between astrocytic processes that invest senile plaques, or alternatively, an aberrant induction of astrocytic Cx43 expression which may further compromise homeostasis and exacerbate pathological conditions in the microenvironment of amyloid plaques.
引用
收藏
页码:173 / 178
页数:6
相关论文
共 21 条