Mécanismes pathogéniques des maladies neurodégénératives: l'exemple de la sclérose latérale amyotrophique [Pathogenic mechanisms of neurodegenerative diseases: amyotrophic lateral sclerosis]
Details
Download: RMS_64_1152.pdf (143.37 [Ko])
State: Public
Version: Final published version
License: CC BY-NC-ND 4.0
State: Public
Version: Final published version
License: CC BY-NC-ND 4.0
Serval ID
serval:BIB_502671862A51
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Mécanismes pathogéniques des maladies neurodégénératives: l'exemple de la sclérose latérale amyotrophique [Pathogenic mechanisms of neurodegenerative diseases: amyotrophic lateral sclerosis]
Journal
Revue medicale suisse
ISSN
1660-9379 (Print)
ISSN-L
1660-9379
Publication state
Published
Issued date
03/05/2006
Peer-reviewed
Oui
Volume
2
Number
64
Pages
1152-1157
Language
french
Notes
Publication types: English Abstract ; Journal Article ; Review
Publication Status: ppublish
Publication Status: ppublish
Abstract
Since its description by Charcot in 1869, the mechanism underlying the characteristic selective degeneration and death of motor neurons in amyotrophic lateral sclerosis (ALS) has remained a mystery. There is no effective remedy for this progressive, fatal disorder. Modern genetics have now identified two genes, SODI and ALS2 as primary causes of the disease and has implicated others as potential contributors. These insights have enabled development of model systems to test hypotheses of disease mechanism and potential therapies. Along with errors in the handling of synaptic glutamate and the potential excitotoxic response that it provokes, these model systems underscore the involvement of non-neuronal cells in disease progression and provide new therapeutic strategies.
Keywords
Amyotrophic Lateral Sclerosis/etiology, Humans
Pubmed
Create date
25/01/2008 12:49
Last modification date
13/12/2024 9:12