Adult Neurogenesis and the Ischemic Forebrain

Lichtenwalner, Robin J.; Parent, Jack M.

doi:10.1038/sj.jcbfm.9600170

Cited by 261 publications

(194 citation statements)

References 210 publications

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“…In neonatal rats with experimental hypoxic-ischemic injury, sustained neurogenesis persists in the subventricular zone for months after injury and continues to populate the cerebral cortex with new neurons [Yang et al, 2007]. A similar phenomenon has been shown to occur in adult rodents after stroke [Lichtenwalner and Parent, 2006]. Newborn neu-rons integrate into existing circuits and could contribute to recovery from injury.…”

Section: Mechanisms For Plasticity In the Central Nervous Systemmentioning

confidence: 87%

Plasticity in the developing brain: Implications for rehabilitation

Johnston

2009

Dev Disabil Res Revs

412

268

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Neuronal plasticity allows the central nervous system to learn skills and remember information, to reorganize neuronal networks in response to environmental stimulation, and to recover from brain and spinal cord injuries. Neuronal plasticity is enhanced in the developing brain and it is usually adaptive and beneficial but can also be maladaptive and responsible for neurological disorders in some situations. Basic mechanisms that are involved in plasticity include neurogenesis, programmed cell death, and activity-dependent synaptic plasticity. Repetitive stimulation of synapses can cause long-term potentiation or long-term depression of neurotransmission. These changes are associated with physical changes in dendritic spines and neuronal circuits. Overproduction of synapses during postnatal development in children contributes to enhanced plasticity by providing an excess of synapses that are pruned during early adolescence. Clinical examples of adaptive neuronal plasticity include reorganization of cortical maps of the fingers in response to practice playing a stringed instrument and constraint-induced movement therapy to improve hemiparesis caused by stroke or cerebral palsy. These forms of plasticity are associated with structural and functional changes in the brain that can be detected with magnetic resonance imaging, positron emission tomography, or transcranial magnetic stimulation (TMS). TMS and other forms of brain stimulation are also being used experimentally to enhance brain plasticity and recovery of function. Plasticity is also influenced by genetic factors such as mutations in brain-derived neuronal growth factor. Understanding brain plasticity provides a basis for developing better therapies to improve outcome from acquired brain injuries. ' 2009 Wiley-Liss, Inc. Dev Disabil Res Rev 200915:94-101.

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Section: Mechanisms For Plasticity In the Central Nervous Systemmentioning

confidence: 87%

Plasticity in the developing brain: Implications for rehabilitation

Johnston

2009

Dev Disabil Res Revs

412

268

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“…However, after stroke and other forms of brain injury, neuroblasts swerve away from their designated path and mi- grate toward damaged tissue instead (Lichtenwalner and Parent, 2005;Zhang et al, 2005). Cell migration requires an active extracellular protease response.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Matrix Metalloproteinase in Neuroblast Cell Migration from the Subventricular Zone after Stroke

Lee¹,

Kim²,

Rogowska³

et al. 2006

J. Neurosci.

255

183

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After brain injury, neuroblast cells from the subventricular zone (SVZ) expand and migrate toward damaged tissue. The mechanisms that mediate these neurogenic and migratory responses remain to be fully dissected. Here, we show that bromodeoxyuridine-labeled and doublecortin-positive cells from the SVZ colocalize with the extracellular protease matrix metalloproteinase-9 (MMP-9) during the 2 week recovery period after transient focal cerebral ischemia in mice. Treatment with the broad spectrum MMP inhibitor GM6001 significantly decreases the migration of doublecortin-positive cells that extend from the SVZ into the striatum. These data suggest that MMPs are involved in endogenous mechanisms of neurogenic migration as the brain seeks to heal itself after injury.

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“…The newly born cells are witnessed to migrate into damaged regions. 120 A vital factor for neurogenesis, survival signalling, and synaptic plasticity in the ischemic hemisphere is brain-derived neurotrophic factor (BDNF). [121][122][123] Histone deacetylase inhibition induces BDNF-receptor tyrosine kinase (TrkB)-dependent cell proliferation, migration, and differentiation in experimental stroke.…”

Section: Neurogenesis and Plasticitymentioning

confidence: 99%

Epigenetic Mechanisms in Cerebral Ischemia

Schweizer

Meisel

Märschenz

2013

J Cereb Blood Flow Metab

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Treatment efficacy for ischemic stroke represents a major challenge. Despite fundamental advances in the understanding of stroke etiology, therapeutic options to improve functional recovery remain limited. However, growing knowledge in the field of epigenetics has dramatically changed our understanding of gene regulation in the last few decades. According to the knowledge gained from animal models, the manipulation of epigenetic players emerges as a highly promising possibility to target diverse neurologic pathologies, including ischemia. By altering transcriptional regulation, epigenetic modifiers can exert influence on all known pathways involved in the complex course of ischemic disease development. Beneficial transcriptional effects range from attenuation of cell death, suppression of inflammatory processes, and enhanced blood flow, to the stimulation of repair mechanisms and increased plasticity. Most striking are the results obtained from pharmacological inhibition of histone deacetylation in animal models of stroke. Multiple studies suggest high remedial qualities even upon late administration of histone deacetylase inhibitors (HDACi). In this review, the role of epigenetic mechanisms, including histone modifications as well as DNA methylation, is discussed in the context of known ischemic pathways of damage, protection, and regeneration.

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Adult Neurogenesis and the Ischemic Forebrain

Cited by 261 publications

References 210 publications

Plasticity in the developing brain: Implications for rehabilitation

Plasticity in the developing brain: Implications for rehabilitation

Involvement of Matrix Metalloproteinase in Neuroblast Cell Migration from the Subventricular Zone after Stroke

Epigenetic Mechanisms in Cerebral Ischemia

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