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Neuronal replacement from endogenous precursors in the adult brain after stroke
It is shown that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone, and stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion.
Inflammation is detrimental for neurogenesis in adult brain
It is demonstrated that lipopolysaccharide-induced inflammation, which gives rise to microglia activation in the area where the new neurons are born, strongly impairs basal hippocampal neurogenesis in rats, raising the possibility that suppression of hippocampal Neurogenesis by activatedmicroglia contributes to cognitive dysfunction in aging, dementia, epilepsy, and other conditions leading to brain inflammation.
Persistent Production of Neurons from Adult Brain Stem Cells During Recovery after Stroke
It is shown that endogenous neural stem cells continuously supply the injured adult brain with new neurons, which suggests novel self‐repair strategies to improve recovery after stroke.
Direct conversion of human fibroblasts to dopaminergic neurons
It is shown that the same strategy can be applied to human embryonic and postnatal fibroblasts and it is demonstrated that the converted neurons can be directed toward distinct functional neurotransmitter phenotypes when the appropriate transcriptional cues are provided together with the three conversion factors.
Forebrain ependymal cells are Notch-dependent and generate neuroblasts and astrocytes after stroke
Although ependymal cells act as primary cells in the neural lineage to produce neurons and glial cells after stroke, they do not fulfill defining criteria for stem cells under these conditions and instead serve as a reservoir that is recruited by injury.
Seizures induce widespread upregulation of cystatin B, the gene mutated in progressive myoclonus epilepsy, in rat forebrain neurons
Findings demonstrate that seizure activity leads to rapid and widespread increases of the synthesis of CSTB in forebrain neurons and propose that the upregulation of CST B following seizures may counteract apoptosis by binding cysteine proteases.
Cell replacement therapies for central nervous system disorders
In animal models, immature neural precursors can replace lost neurons, restore function and promote brain self-repair. Clinical trials in Parkinson's disease suggest that similar approaches may also