Basic fibroblast growth factor does not prolong survival in a transgenic model of familial amyotrophic lateral sclerosis
M. N. Upton-Rice BS
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorM. E. Cudkowicz MD, MSc
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Clinical Trial Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorL. Warren BA
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorR. K. Mathew BA
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorJ. M. Ren MD
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorS. P. Finklestein MD
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorR. H. Brown Jr MD, DPhil
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorM. N. Upton-Rice BS
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorM. E. Cudkowicz MD, MSc
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Clinical Trial Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorL. Warren BA
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorR. K. Mathew BA
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorJ. M. Ren MD
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorS. P. Finklestein MD
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorR. H. Brown Jr MD, DPhil
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA
Search for more papers by this author
References
- 1 Rosen DR, Siddique T, Patterson D, et al. Mutations in Cu/Zn superoxide dismutase are associated with familial amyotrophic lateral sclerosis. Nature 1993; 362: 59–62
- 2
Ay I,
Finkelstein S.
Preclinical trials of basic fibroblast growth factor (bFGF) in animal models of stroke. In:
M Mattson, ed.
Neuroprotective signal transduction.
Totown:
Humana Press,
1998;
111–118.
10.1007/978-1-59259-475-7_6 Google Scholar
- 3 Gurney M, Cutting F, Zhai P, et al. Benefit of vitamin E, riluzole and gabapentin in a transgenic model of familial ALS. Ann Neurol 1996; 39: 147–157
- 4 Klivenyi P, Ferrante R, Matthew R, et al. Neuroprotective effects of creatine in a transgenic animal model of ALS. Nat Med 1999; 5: 347–350
- 5 Hottinger A, Fine E, Gurney M, et al. The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. Eur J Neurosci 1997; 9: 1548–1551