The Value of Transgenic Models for the Study of Neurodegenerative Diseases

: Transgenic animal models are useful in studying the features of APP‐ and PS1‐linked FAD and SOD1‐linked FALS. These models help to investigate the nature of the cellular/biochemical/molecular alterations in neural tissue; the character and evolution of neuronal and/or glial abnormalities; the ways...

Full description

Saved in:
Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2000-12, Vol.920 (1), p.179-191
Main Authors: PRICE, DONALD L., WONG, PHILIP C., MARKOWSKA, ALICJA L., LEE, MICHAEL K., THINAKAREN, GOPAL, CLEVELAND, DONALD W., SISODIA, SANGRAM S., BORCHELT, DAVID R.
Format: Article
Language:English
Subjects:
Alzheimer Disease - genetics
Amyloid beta-Protein Precursor - deficiency
Amyloid beta-Protein Precursor - genetics
Amyloidosis - genetics
Animals
Disease Models, Animal
Humans
Membrane Proteins - genetics
Mice
Mice, Knockout
Mice, Transgenic
Motor Neuron Disease - genetics
Neurodegenerative Diseases - genetics
Neurodegenerative Diseases - pathology
Neurodegenerative Diseases - physiopathology
Presenilin-1
Presenilin-2
Superoxide Dismutase - genetics
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:: Transgenic animal models are useful in studying the features of APP‐ and PS1‐linked FAD and SOD1‐linked FALS. These models help to investigate the nature of the cellular/biochemical/molecular alterations in neural tissue; the character and evolution of neuronal and/or glial abnormalities; the ways mutant proteins cause damage to neurons; and the biochemical pathways associated with cell death. New technologies will help to define changes in a variety of genes/gene products and the events and conformational changes in mutant proteins that are implicated in pathogenic cascades. It is hoped such study will result in novel treatments for testing in transgenic models that can then be translated into new treatments for human neurodegenerative diseases.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.2000.tb06920.x