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Insulin-Like Growth Factor-I Promotes Neurogenesis and Synaptogenesis in the Hippocampal Dentate Gyrus during Postnatal Development

The Journal of neuroscience, 2000-11, Vol.20 (22), p.8435-8442

2000

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Type 1 insulin-like growth factor receptor signaling is essential for the development of the hippocampal formation and dentate gyrus

Journal of neuroscience research, 2009-10, Vol.87 (13), p.2821-2832

2009

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In vivo effects of insulin-like growth factor-I (IGF-I) on prenatal and early postnatal development of the central nervous system

The European journal of neuroscience, 2004-04, Vol.19 (8), p.2056-2068

2004

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Neurodevelopmental effects of insulin-like growth factor signaling

Frontiers in neuroendocrinology, 2012-08, Vol.33 (3), p.230-251

2012

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Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G1 Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

The Journal of neuroscience, 2004-11, Vol.24 (45), p.10201-10210

2004

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Mutant mouse models of insulin-like growth factor actions in the central nervous system

Neuropeptides (Edinburgh), 2002-04, Vol.36 (2-3), p.209-220

2002

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Signalling through the type 1 insulin-like growth factor receptor (IGF1R) interacts with canonical Wnt signalling to promote neural proliferation in developing brain

ASN neuro, 2012-07, Vol.4 (5), p.AN20120009

2012

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Targeted disruption of the Huntington's disease gene results in embryonic lethality and behavioral and morphological changes in heterozygotes

Cell, 1995-06, Vol.81 (5), p.811-823

1995

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Maternal Dietary (n-3) Fatty Acid Deficiency Alters Neurogenesis in the Embryonic Rat Brain

The Journal of nutrition, 2006-06, Vol.136 (6), p.1570-1575

2006

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Human Retinal Pigment Epithelial Cell Implants Ameliorate Motor Deficits in Two Rat Models of Parkinson Disease

Journal of neuropathology and experimental neurology, 2007-07, Vol.66 (7), p.576-584

2007

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Characterization and Survival of Long-Term Implants of Human Retinal Pigment Epithelial Cells Attached to Gelatin Microcarriers in a Model of Parkinson Disease

Journal of neuropathology and experimental neurology, 2007-07, Vol.66 (7), p.585-596

2007

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Neuronal degeneration in the basal ganglia and loss of pallido-subthalamic synapses in mice with targeted disruption of the Huntington's disease gene

Brain research, 1999-02, Vol.818 (2), p.468-479

1999

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Single Inflammatory Trigger Leads to Neuroinflammation in LRRK2 Rodent Model without Degeneration of Dopaminergic Neurons

Journal of Parkinson's disease, 2019-01, Vol.9 (1), p.121-139

2019

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Insulin‐like growth factor‐I (IGF‐I) inhibits neuronal apoptosis in the developing cerebral cortex in vivo

International journal of developmental neuroscience, 2007-06, Vol.25 (4), p.233-241

2007

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Increased expression of insulin-like growth factor-I (IGF-I) during embryonic development produces neocortical overgrowth with differentially greater effects on specific cytoarchitectonic areas and cortical layers

Brain research. Developmental brain research, 2005-02, Vol.154 (2), p.227-237

2005

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Increased insulin-like growth factor-I (IGF-I) expression during early postnatal development differentially increases neuron number and growth in medullary nuclei of the mouse

Brain research. Developmental brain research, 1999-04, Vol.114 (1), p.135-141

1999

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Postnatal changes in the numerical density and total number of asymmetric and symmetric synapses in the hypoglossal nucleus of the rat

Brain research. Developmental brain research, 1998-06, Vol.108 (1), p.179-191

O'Kusky, John R

1998

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Effects of d-3-hydroxybutyrate treatment on hypoglycemic coma in rat pups

Experimental neurology, 2011-01, Vol.227 (1), p.180-187

2011

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Maternal Dietary (n-3) Fatty Acid Deficiency Alters Neurogenesis in the Embryonic Rat Brain1,2

The Journal of nutrition, 2006-06, Vol.136 (6), p.1570

2006

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Increased expression of insulin-like growth factor I augments the progressive phase of synaptogenesis without preventing synapse elimination in the hypoglossal nucleus

Journal of comparative neurology (1911), 2003-09, Vol.464 (3), p.382-391

2003

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Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G sub(1) Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

The Journal of neuroscience, 2004-11, Vol.24 (45), p.10201-10210

2004

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Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G 1 Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

The Journal of neuroscience, 2004-11, Vol.24 (45), p.10201-10210

2004

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Sudden Infant Death Syndrome: Increased Number of Synapses in the Hypoglossal Nucleus

Journal of neuropathology and experimental neurology, 1995-09, Vol.54 (5), p.627-634

1995

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Toward Understanding the Molecular Pathology of Huntington's Disease

Brain pathology (Zurich, Switzerland), 1997-07, Vol.7 (3), p.979-1002

1997

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Sudden Infant Death Syndrome: Increased Synaptic Density in the Central Reticular Nucleus of the Medulla

Journal of neuropathology and experimental neurology, 1994-05, Vol.53 (3), p.263-271

1994

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Insulin-Like Growth Factor-I Promotes Neurogenesis and Synaptogenesis in the Hippocampal Dentate Gyrus during Postnatal Development

Type 1 insulin-like growth factor receptor signaling is essential for the development of the hippocampal formation and dentate gyrus

In vivo effects of insulin-like growth factor-I (IGF-I) on prenatal and early postnatal development of the central nervous system

Neurodevelopmental effects of insulin-like growth factor signaling

Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G1 Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

Mutant mouse models of insulin-like growth factor actions in the central nervous system

Signalling through the type 1 insulin-like growth factor receptor (IGF1R) interacts with canonical Wnt signalling to promote neural proliferation in developing brain

Targeted disruption of the Huntington's disease gene results in embryonic lethality and behavioral and morphological changes in heterozygotes

Maternal Dietary (n-3) Fatty Acid Deficiency Alters Neurogenesis in the Embryonic Rat Brain

Human Retinal Pigment Epithelial Cell Implants Ameliorate Motor Deficits in Two Rat Models of Parkinson Disease

Characterization and Survival of Long-Term Implants of Human Retinal Pigment Epithelial Cells Attached to Gelatin Microcarriers in a Model of Parkinson Disease

Neuronal degeneration in the basal ganglia and loss of pallido-subthalamic synapses in mice with targeted disruption of the Huntington's disease gene

Single Inflammatory Trigger Leads to Neuroinflammation in LRRK2 Rodent Model without Degeneration of Dopaminergic Neurons

Insulin‐like growth factor‐I (IGF‐I) inhibits neuronal apoptosis in the developing cerebral cortex in vivo

Increased expression of insulin-like growth factor-I (IGF-I) during embryonic development produces neocortical overgrowth with differentially greater effects on specific cytoarchitectonic areas and cortical layers

Increased insulin-like growth factor-I (IGF-I) expression during early postnatal development differentially increases neuron number and growth in medullary nuclei of the mouse

Postnatal changes in the numerical density and total number of asymmetric and symmetric synapses in the hypoglossal nucleus of the rat

Effects of d-3-hydroxybutyrate treatment on hypoglycemic coma in rat pups

Maternal Dietary (n-3) Fatty Acid Deficiency Alters Neurogenesis in the Embryonic Rat Brain1,2

Increased expression of insulin-like growth factor I augments the progressive phase of synaptogenesis without preventing synapse elimination in the hypoglossal nucleus

Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G sub(1) Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

Insulin-Like Growth Factor-I Accelerates the Cell Cycle by Decreasing G 1 Phase Length and Increases Cell Cycle Reentry in the Embryonic Cerebral Cortex

Sudden Infant Death Syndrome: Increased Number of Synapses in the Hypoglossal Nucleus

Toward Understanding the Molecular Pathology of Huntington's Disease

Sudden Infant Death Syndrome: Increased Synaptic Density in the Central Reticular Nucleus of the Medulla

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