Chronic cognitive deficits and amyloid precursor protein elevation after selective immunotoxin lesions of the basal forebrain cholinergic system

被引：48

作者：

Lin, L ^{[1
]}

LeBlanc, CJ ^{[1
]}

Deacon, TW ^{[1
]}

Isacson, O ^{[1
]}

机构：

[1] Harvard Univ, McLean Hosp, Sch Med, Neuroregenerat Lab, Belmont, MA 02178 USA

来源：

NEUROREPORT | 1998年 / 9卷 / 03期

关键词：

Alzheimer's disease; amyloid precursor protein; cholinergic system; immunolesion; beta-peptide;

D O I：

10.1097/00001756-199802160-00030

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

ALZHEIMER'S disease (AD) is the most common neurodegenerative disorder that causes cognitive deficits in the elderly. Its neuropathology is characterized by amyloid deposition and specific cholinergic degeneration. To address the link between amyloid formation and cholinergic loss, we examined histologically the amyloid precursor protein (APP) changes following selective immunolesion of the basal forebrain cholinergic system with 192 IgG-saporin in rats at 6 months post-lesion. In such rats with cognitive deficits observed in Morris water maze tests, we found increased levels of APP by optical density measurements in regions of cholinergic denervation. APP elevation and performance in the water maze task correlate with reduction of acetylcholinesterase (AChE) activity in the frontal cortex and CA3 subfield of hippocampus. The data indicate that loss of cholinergic innervation can affect APP expression.

引用

页码：547 / 552

页数：6

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