Copaxone in Age Related Macular Degeneration
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|ClinicalTrials.gov Identifier: NCT00466076|
Recruitment Status : Unknown
Verified April 2007 by Kaplan Medical Center.
Recruitment status was: Recruiting
First Posted : April 27, 2007
Last Update Posted : April 27, 2007
|Condition or disease||Intervention/treatment||Phase|
|Macular Degeneration||Drug: Copaxone (Glatiramer acetate)||Phase 2 Phase 3|
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 Alzheimer’s 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 mouse/human amyloid precursor protein (mice Alzheimer’s 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 Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||30 participants|
|Intervention Model:||Parallel Assignment|
|Official Title:||Subcutaneous Copaxone as Treatment for Dry Age Related Macular Degeneration|
|Study Start Date :||August 2006|
|Estimated Study Completion Date :||April 2007|
- Total drusen area reduction
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00466076
|Contact: Ayala Pollack, MD||972-8-9441353||Ayala_P@clalit.org.il|
|Contact: Gennady Landa, MDfirstname.lastname@example.org|
|Department of Ophthalmology, Kaplan Medical Center||Recruiting|
|Rehovot, Israel, 76100|
|Contact: Annat Pilpoul 972-8-9441691 email@example.com|
|Principal Investigator:||Ayala Pollack, MD||Kaplan Medical Center|