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Trial record 44 of 120 for:    COP1

Copaxone in Age Related Macular Degeneration

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. 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
Information provided by:
Kaplan Medical Center

Tracking Information
First Submitted Date  ICMJE April 25, 2007
First Posted Date  ICMJE April 27, 2007
Last Update Posted Date April 27, 2007
Study Start Date  ICMJE August 2006
Primary Completion Date Not Provided
Current Primary Outcome Measures  ICMJE
 (submitted: April 25, 2007)
Total drusen area reduction
Original Primary Outcome Measures  ICMJE Same as current
Change History No Changes Posted
Current Secondary Outcome Measures  ICMJE Not Provided
Original Secondary Outcome Measures  ICMJE Not Provided
Current Other Pre-specified Outcome Measures Not Provided
Original Other Pre-specified Outcome Measures Not Provided
Descriptive Information
Brief Title  ICMJE Copaxone in Age Related Macular Degeneration
Official Title  ICMJE Subcutaneous Copaxone as Treatment for Dry Age Related Macular Degeneration
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 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  ICMJE Interventional
Study Phase  ICMJE Phase 2
Phase 3
Study Design  ICMJE Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Single
Primary Purpose: Treatment
Condition  ICMJE Macular Degeneration
Intervention  ICMJE Drug: Copaxone (Glatiramer acetate)
Study Arms  ICMJE Not Provided
Publications * Not Provided

*   Includes publications given by the data provider as well as publications identified by Identifier (NCT Number) in Medline.
Recruitment Information
Recruitment Status  ICMJE Unknown status
Enrollment  ICMJE
 (submitted: April 25, 2007)
Original Enrollment  ICMJE Same as current
Estimated Study Completion Date  ICMJE April 2007
Primary Completion Date Not Provided
Eligibility Criteria  ICMJE

Inclusion Criteria:

  1. Dry AMD in both eyes
  2. Age 50 or above.
  3. Signed informed consent.

Exclusion Criteria:

  1. Known sensitivity to mannitol or Copaxone.
  2. Skin disease or active infection of skin.
  3. Active fever or active treatment for infection.
  4. History of other active disaese.
  5. Premenapausal females not using relibale birth control.
  6. Sensitivity for flourescein or iodine.
  7. Inability to comply with study procedures.
Sex/Gender  ICMJE
Sexes Eligible for Study: All
Ages  ICMJE 50 Years and older   (Adult, Older Adult)
Accepts Healthy Volunteers  ICMJE No
Contacts  ICMJE Contact information is only displayed when the study is recruiting subjects
Listed Location Countries  ICMJE Israel
Removed Location Countries  
Administrative Information
NCT Number  ICMJE NCT00466076
Other Study ID Numbers  ICMJE kmc060033
Has Data Monitoring Committee No
U.S. FDA-regulated Product Not Provided
IPD Sharing Statement  ICMJE Not Provided
Responsible Party Not Provided
Study Sponsor  ICMJE Kaplan Medical Center
Collaborators  ICMJE Not Provided
Investigators  ICMJE
Principal Investigator: Ayala Pollack, MD Kaplan Medical Center
PRS Account Kaplan Medical Center
Verification Date April 2007

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP