Copaxone in Age Related Macular Degeneration

The recruitment status of this study is unknown because the information has not been verified recently.
Verified April 2007 by Kaplan Medical Center.
Recruitment status was  Recruiting
Sponsor:
Information provided by:
Kaplan Medical Center
ClinicalTrials.gov Identifier:
NCT00466076
First received: April 25, 2007
Last updated: NA
Last verified: April 2007
History: No changes posted
  Purpose

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


Condition Intervention Phase
Macular Degeneration
Drug: Copaxone (Glatiramer acetate)
Phase 2
Phase 3

Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Masking: Single Blind
Primary Purpose: Treatment
Official Title: Subcutaneous Copaxone as Treatment for Dry Age Related Macular Degeneration

Resource links provided by NLM:


Further study details as provided by Kaplan Medical Center:

Primary Outcome Measures:
  • Total drusen area reduction

Estimated Enrollment: 30
Study Start Date: August 2006
Estimated Study Completion Date: April 2007
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.

  Eligibility

Ages Eligible for Study:   50 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

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.
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00466076

Contacts
Contact: Ayala Pollack, MD 972-8-9441353 Ayala_P@clalit.org.il
Contact: Gennady Landa, MD 972-8-9441353 doctor.landa@gmail.com

Locations
Israel
Department of Ophthalmology, Kaplan Medical Center Recruiting
Rehovot, Israel, 76100
Contact: Annat Pilpoul    972-8-9441691    apilpoul@yahoo.com   
Sponsors and Collaborators
Kaplan Medical Center
Investigators
Principal Investigator: Ayala Pollack, MD Kaplan Medical Center
  More Information

No publications provided

ClinicalTrials.gov Identifier: NCT00466076     History of Changes
Other Study ID Numbers: kmc060033
Study First Received: April 25, 2007
Last Updated: April 25, 2007
Health Authority: Israel: Ethics Commission

Keywords provided by Kaplan Medical Center:
Drusen
AMD
Dry form of Age related Macular Degeneration

Additional relevant MeSH terms:
Macular Degeneration
Retinal Degeneration
Retinal Diseases
Eye Diseases
Copolymer 1
Adjuvants, Immunologic
Immunologic Factors
Physiological Effects of Drugs
Pharmacologic Actions
Immunosuppressive Agents

ClinicalTrials.gov processed this record on September 14, 2014