Abstract
Blocking axonal growth inhibitor NogoA has been of great interest for promoting axonal recovery from neurological diseases. The present study investigates the therapeutic effects of blocking NogoA, inducing functional recovery and promoting white matter repair in an experimental animal model of stroke. Adult male rats were subjected to white matter injury by subcortical ischemic stroke. Twenty-four hours after surgery, 250 ug of anti-NogoA or anti-IgG-1 were administered through the tail vein. The quantity of NogoA protein was determined by immunohistochemistry in the brain and peripheral organs. In addition, functional status, lesion size, fiber tract integrity, axonal sprouting and white matter repair markers were analyzed. Moreover, an in vitro study was performed in order to strengthen the results obtained in vivo. A lower quantity of NogoA protein was found in the brain and peripheral organs of the animals that received anti-NogoA treatment. The animals receiving anti-NogoA treatment showed significantly better results in terms of functional recovery, fiber tract integrity, axonal sprouting and white matter repair markers compared with the control group at 28 days. White matter integrity was in part restored by antibody-mediated inhibition of NogoA administration in those animals that were subjected to an axonal injury by subcortical stroke. This white matter restoration triggered functional recovery.
Highlights
The ability of the adult brain to repair white matter lesions after damage is limited
We found colabeling between NogoA protein and glial fibrillary acidic protein (GFAP), MAP-2, oligodendrocyte transcription factor-2 (Olig-2) and ionized calcium-binding adapter molecule 1 (IBA-1) at 24 h after anti-NogoA administration (Fig. 2D)
White matter injury and the mechanisms of nerve fiber repair have seldom been investigated in translational stroke research[11]
Summary
The ability of the adult brain to repair white matter lesions after damage is limited This lack of ability might be due, at least in part, to molecules that limit axonal growth, such as myelin-associated inhibitors. Blocking NogoA has been of great interest in recent years because it might promote axonal regeneration after white matter damage. In this sense, antibodies that target NogoA have been shown to promote neurite maturation in vitro, axonal growth and functional recovery after cortical stroke[8,9,10] and could be a good therapeutic treatment for white matter ischemic damage. The aim of this study was to investigate the possible therapeutic effects of anti-NogoA in an experimental animal model of subcortical stroke
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