Ignite Creation Date:
2024-05-05 @ 5:29 PM
Last Modification Date:
2024-10-26 @ 9:32 AM
Study NCT ID:
NCT00466076
Status:
UNKNOWN
Last Update Posted:
2007-04-27
First Post:
2007-04-25
Brief Title:
Copaxone in Age Related Macular Degeneration
Sponsor:
Kaplan Medical Center
Organization:
Kaplan Medical Center
Study Overview
Official Title:
Subcutaneous Copaxone as Treatment for Dry Age Related Macular Degeneration
Status:
UNKNOWN
Status Verified Date:
2007-04
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The purpose of the project is to investigate in eyes with dry AMD the efficacy and safety as preventive therapy of the immunomodulatory substance named copaxone which had been proven as safe and effective agent for a neurodegenerative disease in arresting the progression as well as the conversion of dry AMD to wet AMD The hypothesis that the immunomodulatory agent copaxone proven for a neurodegenerative disease may work in the eye is revolutionary and may open a new avenue of preventive treatment for the disease which is the major cause of legal blindness in the industrial world
Detailed Description:
The formation of insoluble extracellular deposits consisting of misfolded aggregated protein is the hallmark of many neurodegenerative diseases Age-related macular degeneration AMD is a degenerative disease in the eye associated with extracellur deposits named drusen Recent evidence suggests that drusen formation and AMD share some similarities with another neurodegenerative disease named Alzheimers disease AD which is associated with amyloid deposits AMD and AD are strongly correlated with advancing age and the formation of amyloid deposits In addition inflammatory mediators and in particular activated microglia are present in amyloid deposits as well as in drusen suggesting a possible common role for the inflammatory pathway in AMD and amyloid diseases Moreover Ambati et al described a new model of AMD in transgenic mice when an absence of normally functioning macrophages led to the development of clinical AMD
Michal Schwartz and her group have recently shown that aggregated b-amyloid Ab induces microglia to become cytotoxic and block neurogenesis from adult rodent neural progenitor cells NPCs IL-4 reversed the impediment attenuated TNF-a production and overcame blockage of insulin like growth factor IGF-I production caused by Ab The significance of microglia for in-vivo neural cell renewal was demonstrated by enhanced neurogenesis in the rat dentate gyrus after injection of IL-4-activated microglia intracerebroventricularly and by the presence of IGF-I-expressing microglia in the dentate gyrus of rats kept in an enriched environment or in the animal model of multiple sclerosis MS Using double-transgenic mice expressing mutant human genes encoding presenilin 1 and chimeric mousehuman amyloid precursor protein mice Alzheimers disease model the group of Michal Schwartz showed that modulation of microglia into dendritic-like cells achieved by a T cell-based vaccination with Copolymer-1 Copaxone resulted in reduction of cognitive decline elimination of plaque formation and induction of neuronal survival and neurogenesis These results introduce a new microglia phenotype as necessary players in fighting off neurodegenerative conditions such as AD and AMD
Michal Schwartz and her group have recently shown that aggregated b-amyloid Ab induces microglia to become cytotoxic and block neurogenesis from adult rodent neural progenitor cells NPCs IL-4 reversed the impediment attenuated TNF-a production and overcame blockage of insulin like growth factor IGF-I production caused by Ab The significance of microglia for in-vivo neural cell renewal was demonstrated by enhanced neurogenesis in the rat dentate gyrus after injection of IL-4-activated microglia intracerebroventricularly and by the presence of IGF-I-expressing microglia in the dentate gyrus of rats kept in an enriched environment or in the animal model of multiple sclerosis MS Using double-transgenic mice expressing mutant human genes encoding presenilin 1 and chimeric mousehuman amyloid precursor protein mice Alzheimers disease model the group of Michal Schwartz showed that modulation of microglia into dendritic-like cells achieved by a T cell-based vaccination with Copolymer-1 Copaxone resulted in reduction of cognitive decline elimination of plaque formation and induction of neuronal survival and neurogenesis These results introduce a new microglia phenotype as necessary players in fighting off neurodegenerative conditions such as AD and AMD
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None