Delayed Administration of a Small Molecule Tropomyosin-Related Kinase B Ligand Promotes Recovery After Hypoxic–Ischemic Stroke
Author(s) -
Jullet Han,
Julia Pollak,
Tao Yang,
Mohammad R. Siddiqui,
Kristian P. Doyle,
Kereshmeh TaravoshLahn,
Egle Cekanaviciute,
Alex Han,
Jeremy Goodman,
Britta E. Jones,
Deqiang Jing,
Stephen M. Massa,
Frank M. Longo,
Marion S. Buckwalter
Publication year - 2012
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.111.641878
Subject(s) - neurogenesis , medicine , stroke (engine) , neuroprotection , neurotrophic factors , neuroplasticity , tropomyosin receptor kinase b , neurotrophin , neuroscience , stroke recovery , brain derived neurotrophic factor , angiogenesis , receptor , pharmacology , biology , physical therapy , rehabilitation , mechanical engineering , psychiatry , engineering
Stroke is the leading cause of long-term disability in the United States, yet no drugs are available that are proven to improve recovery. Brain-derived neurotrophic factor stimulates neurogenesis and plasticity, processes that are implicated in stroke recovery. It binds to both the tropomyosin-related kinase B and p75 neurotrophin receptors. However, brain-derived neurotrophic factor is not a feasible therapeutic agent, and no small molecule exists that can reproduce its binding to both receptors. We tested the hypothesis that a small molecule (LM22A-4) that selectively targets tropomyosin-related kinase B would promote neurogenesis and functional recovery after stroke.
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