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Neuronal replacement from endogenous precursors in the adult brain after stroke
TLDR
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
TLDR
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
TLDR
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.
BDNF-induced TrkB activation down-regulates the K+–Cl− cotransporter KCC2 and impairs neuronal Cl− extrusion
TLDR
It is shown that exposure of rat hippocampal slice cultures and acute slices to exogenous BDNF or neurotrophin-4 produces a TrkB-mediated fall in the neuron-specific K+–Cl− cotransporter KCC2 mRNA and protein, as well as a consequent impairment in neuronal Cl− extrusion capacity.
Forebrain ependymal cells are Notch-dependent and generate neuroblasts and astrocytes after stroke
TLDR
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
TLDR
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.
Apoptosis and proliferation of dentate gyrus neurons after single and intermittent limbic seizures.
TLDR
The present data show that single and intermittent, brief seizures induce both apoptotic death and proliferation of dentate gyrus neurons, and it is hypothesized that these processes, occurring early during epileptogenesis, are primary events in the development of hippocampal pathology in animals and possibly also in patients suffering from temporal lobe epilepsy.
Tumor Necrosis Factor Receptor 1 Is a Negative Regulator of Progenitor Proliferation in Adult Hippocampal Neurogenesis
Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine, acting through the TNF-R1 and TNF-R2 receptors. The two receptors have been proposed to mediate distinct TNF-α effects in the CNS,
A latent neurogenic program in astrocytes regulated by Notch signaling in the mouse
TLDR
Working in mice, Magnusson et al. hunted for intrinsic genetic programs that can help adult brains produce replacement neurons and found that astrocytes, spidery cells that are interspersed between neurons, carry a latent neurogenic program that may be useful for neuronal replacement strategies.
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