C3 and f.B deficient mice as a tole to study the role of the complement system in the pathogenesis of AD

C3 and f.B deficient mice as a tole to study the role of the complement system in the pathogenesis of AD

Field: Disorders of the nervous system

Authors: Nilsson, Ann-Katrin
Persson, Linda
Hietala, Albert
Pekna, Marcela

Address of presenting
author: Ann-Katrin Nilsson
Inst. för medicinsk och fysiologisk kemi
Göteborgs Universitet
Box 440
405 30 Göteborg

E-mail: Ann-Katrin.Nilsson@medkem.gu.se

Phone: 031-773 3465

Fax: 031-416 108

Text of abstract: C3 AND FACTOR B DEFICIENT MICE GENERATED BY GENE TARGETING AS A TOOL TO STUDY THE ROLE OF THE COMPLEMENT SYSTEM IN THE PATHOGENESIS OF ALZHEIMER'S DISEASE
A-K. Nilsson, L. Persson, A. Hietala, M. Pekna
Dept. of Medical Biochemistry, University of Göteborg, Medicinaregatan 9, S-405 30 Göteborg, Sweden
Alzheimer's disease is the fourth leading cause of death in the developed world after myocardial infarction, cancer and stroke and it is realistic to foresee that the incidence of this disease will continue to increase with the population aging. Alzheimer's disease is a progressive dementing illness causing neurodegeneration in selective regions of the forebrain. The histological features include senile plaques, neurofibrillary tangles, dystrophic neurites and amyloid formation. The pathogenesis of Alzheimer's disease is, despite of a substantial progress during the past several years, only partially understood. The deposits of b-amyloid in the cortex and hippocampus seem to be necessary but not sufficient for the neurodegeneration and dementia of Alzheimer's diseases. There is increasing evidence that inflammatory reaction, oxidative damage by free radicals and reactive gliosis may play an important role in the pathogenesis of this disease. The efficient prevention and treatment of Alzheimer's disease depends on the understanding of its pathogenesis. New research tools have recently become available which can be used to study aspects of Alzheimer's disease pathogenesis at a level which was not accessible before. By using transgenic technology (gene targeting), we have developed animal models which enable us to address the role of the complement system in the neurodegeneration and memory loss associated with Alzheimer's disease.

Keywords: complement, Alzheimer's disease

	C3 and f.B deficient mice as a tole to study the role of the complement system in the pathogenesis of AD
Field:	Disorders of the nervous system
Authors:	Nilsson, Ann-Katrin Persson, Linda Hietala, Albert Pekna, Marcela
Address of presenting author:	Ann-Katrin Nilsson Inst. för medicinsk och fysiologisk kemi Göteborgs Universitet Box 440 405 30 Göteborg
E-mail:	Ann-Katrin.Nilsson@medkem.gu.se
Phone:	031-773 3465
Fax:	031-416 108
Text of abstract:	C3 AND FACTOR B DEFICIENT MICE GENERATED BY GENE TARGETING AS A TOOL TO STUDY THE ROLE OF THE COMPLEMENT SYSTEM IN THE PATHOGENESIS OF ALZHEIMER'S DISEASE A-K. Nilsson, L. Persson, A. Hietala, M. Pekna Dept. of Medical Biochemistry, University of Göteborg, Medicinaregatan 9, S-405 30 Göteborg, Sweden Alzheimer's disease is the fourth leading cause of death in the developed world after myocardial infarction, cancer and stroke and it is realistic to foresee that the incidence of this disease will continue to increase with the population aging. Alzheimer's disease is a progressive dementing illness causing neurodegeneration in selective regions of the forebrain. The histological features include senile plaques, neurofibrillary tangles, dystrophic neurites and amyloid formation. The pathogenesis of Alzheimer's disease is, despite of a substantial progress during the past several years, only partially understood. The deposits of b-amyloid in the cortex and hippocampus seem to be necessary but not sufficient for the neurodegeneration and dementia of Alzheimer's diseases. There is increasing evidence that inflammatory reaction, oxidative damage by free radicals and reactive gliosis may play an important role in the pathogenesis of this disease. The efficient prevention and treatment of Alzheimer's disease depends on the understanding of its pathogenesis. New research tools have recently become available which can be used to study aspects of Alzheimer's disease pathogenesis at a level which was not accessible before. By using transgenic technology (gene targeting), we have developed animal models which enable us to address the role of the complement system in the neurodegeneration and memory loss associated with Alzheimer's disease.

Keywords:	complement, Alzheimer's disease

Index

Created 2000-03-15

Department of Physiological Sciences, Lund University

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