Table 1.
Type of Injury | Type of NSCs and Species | Region and Timing of grafting | Effect on Memory Function | Effect on Mood Function |
---|---|---|---|---|
KA-induced unilateral hippocampal injury in rat [39] | NSCs from the postnatal SVZ | Injured CA3 Region at 5 days after injury | Prevented spatial and recognition memory deficits | Prevented depressive-like behavior |
KA-induced bilateral hippocampal injury in mouse [60] | NSCs from the postnatal SVZ transduced with IGF-1 | Injured hippocampus at 4 days after injury | Reduced Memory Deficits | Not Examined |
KA-induced unilateral hippocampal injury in rat [64] | Human NSCs transduced with ChAT | Injured hippocampus at 4 weeks after injury | Improved memory function | Not examined |
Fluid Percussion prototype of TBI in rat [61] | Human fetal NSCs | Injured hippocampus one-day after TBI | Improved Memory Function | Not examined |
Triple transgenic AD mouse (3xTg-AD) [38] | NSCs from the entire postnatal day 1 brain | hippocampus of 18-month old mice exhibiting Aβ plaques and NFTs | Improved Memory Function | Not examined |
Status epilepticus (SE) induced hippocampal injury in rat [40] | NSCs from the postnatal SVZ | Injured hippocampi (bilateral) 7-days after SE | Prevented recognition memory dysfunction | Prevented depressive-like behavior |
Aβ, amyloid beta; AD, Alzheimer’s disease; BDNF, brain derived neurotrophic factor; ChAT, choline acetyltransferase; GD, gestation day; IGF-1, insulin-like growth factor-1; KA, kainic acid; NFTs, neurofibrillary tangles; NSCs, neural stem cells; SE, status epilepticus; SVZ, subventricular zone; TBI, traumatic brain injury.