Antisense therapy in a rat model of Alexander disease reverses GFAP pathology, white matter deficits, and motor impairment

Author:

Hagemann Tracy L.1ORCID,Powers Berit2,Lin Ni-Hsuan3ORCID,Mohamed Ahmed F.1,Dague Katerina L.1ORCID,Hannah Seth C.1,Bachmann Gemma2ORCID,Mazur Curt2ORCID,Rigo Frank2,Olsen Abby L.4ORCID,Feany Mel B.5ORCID,Perng Ming-Der3ORCID,Berman Robert F.6ORCID,Messing Albee17ORCID

Affiliation:

1. Waisman Center, University of Wisconsin-Madison, Madison, WI 53705, USA.

2. Ionis Pharmaceuticals, Carlsbad, CA 92010, USA.

3. Institute of Molecular Medicine, College of Life Sciences, National Tsing Hua University, Hsinchu 30013, Taiwan.

4. Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA.

5. Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA.

6. Department of Neurological Surgery and M.I.N.D Institute, University of California, Davis, Davis, CA 95616, USA.

7. Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53705, USA.

Abstract

Gfap -antisense prevents disease with early treatment and reverses clinical phenotypes with late treatment in a rat model of Alexander disease.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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