Table 3.
Potential targets to augment neural repair after stroke.
| Target | Example |
|---|---|
| Gray matter | |
| Axonal sprouting | Inosine, PDE inhibitors, Growth factors, Stem cells |
| Dendritic branching | CCR5 blockade, Growth factors, Stem cells |
| Neurogenesis | Cerebrolysin, Growth factors, Stem cells |
| Angiogenesis | Growth factors, Stem cells |
| White matter | |
| Axon preservation | MCT-1 augmentation, NMNAT1/DLK/STAT3 manipulation |
| Remyelination | OPC proliferation/differentiation, Nogo blockade |
| Blood brain barrier | Endothelial cell metabolism, Pericyte proliferation |
| Microglia | TLR4 inhibition, Manipulating activation state |
| Glial scar | |
| Myelin-associated proteins | Nogo, MAG, MOBP blockade |
| Extracellular matrix proteins | Chondroitin sulfate proteoglycan inhibition |
| Growth cone inhibitors | Semaphorin, Eprhin blockade |
| Excitability | |
| Alter inhibition pharmacologically | SSRIs, CREB induction, GABA antagonism, Zolpidem, Amphetamines, L-dopa |
| Alter inhibition neurotechnologically | Transcranial magnetic stimulation, transcranial direct current stimulation, Deep brain stimulation, Vagal nerve stimulation |
| Brain cortical maps and networks | |
|
Macro level changes that depend may on changes in structure/excitability |
Rehabilitation: physical, occupational, speech Activity-based therapies, Sensory stimulation, Robot-based therapies Cognitive strategies, Functional MRI, Virtual reality Brain computer interfaces, C7 nerve root transfer |