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GSK-3β overexpression causes reversible alterations on postsynaptic densities and dendritic morphology of hippocampal granule neurons in vivo
by
Hernández, F
, Ávila, J
, Ulloa, F
, Rábano, A
, Llorens-Martín, M
, Jurado-Arjona, J
, Soriano, E
, deFelipe, J
, Teixeira, C M
, Fuster-Matanzo, A
in
631/378/368
/ 692/699/375/365/1283
/ Adult and adolescent clinical studies
/ Alzheimer Disease - enzymology
/ Alzheimer Disease - genetics
/ Alzheimer Disease - physiopathology
/ Alzheimer's disease
/ Animal models
/ Animals
/ Behavioral Sciences
/ Biological and medical sciences
/ Biological Psychology
/ Data processing
/ Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
/ Dendrites - ultrastructure
/ Dendritic branching
/ Enrichment
/ Environment
/ Glycogen
/ Glycogen synthase kinase 3
/ Glycogen Synthase Kinase 3 - biosynthesis
/ Glycogen Synthase Kinase 3 - genetics
/ Glycogen Synthase Kinase 3 beta
/ Granule cells
/ Hippocampal plasticity
/ Hippocampus
/ Hippocampus (Brain)
/ Hippocampus - anatomy & histology
/ Hippocampus - enzymology
/ Hippocampus - physiology
/ Humans
/ Medical sciences
/ Medicine
/ Medicine & Public Health
/ Memory
/ Mice
/ Mice, Transgenic
/ Morphology
/ Neonates
/ Neurodegenerative diseases
/ Neurogenesis
/ Neurogenesis - physiology
/ Neurology
/ Neurons
/ Neurons - cytology
/ Neurons - physiology
/ Neurosciences
/ Organic mental disorders. Neuropsychology
/ original-article
/ Pharmacotherapy
/ Physiological aspects
/ Plasticity (hippocampal)
/ Post-Synaptic Density - ultrastructure
/ postsynaptic density
/ Postsynaptic density proteins
/ Protein kinases
/ Psychiatry
/ Psychology. Psychoanalysis. Psychiatry
/ Psychopathology. Psychiatry
/ Retrovirus
/ Up-Regulation
2013
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GSK-3β overexpression causes reversible alterations on postsynaptic densities and dendritic morphology of hippocampal granule neurons in vivo
by
Hernández, F
, Ávila, J
, Ulloa, F
, Rábano, A
, Llorens-Martín, M
, Jurado-Arjona, J
, Soriano, E
, deFelipe, J
, Teixeira, C M
, Fuster-Matanzo, A
in
631/378/368
/ 692/699/375/365/1283
/ Adult and adolescent clinical studies
/ Alzheimer Disease - enzymology
/ Alzheimer Disease - genetics
/ Alzheimer Disease - physiopathology
/ Alzheimer's disease
/ Animal models
/ Animals
/ Behavioral Sciences
/ Biological and medical sciences
/ Biological Psychology
/ Data processing
/ Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
/ Dendrites - ultrastructure
/ Dendritic branching
/ Enrichment
/ Environment
/ Glycogen
/ Glycogen synthase kinase 3
/ Glycogen Synthase Kinase 3 - biosynthesis
/ Glycogen Synthase Kinase 3 - genetics
/ Glycogen Synthase Kinase 3 beta
/ Granule cells
/ Hippocampal plasticity
/ Hippocampus
/ Hippocampus (Brain)
/ Hippocampus - anatomy & histology
/ Hippocampus - enzymology
/ Hippocampus - physiology
/ Humans
/ Medical sciences
/ Medicine
/ Medicine & Public Health
/ Memory
/ Mice
/ Mice, Transgenic
/ Morphology
/ Neonates
/ Neurodegenerative diseases
/ Neurogenesis
/ Neurogenesis - physiology
/ Neurology
/ Neurons
/ Neurons - cytology
/ Neurons - physiology
/ Neurosciences
/ Organic mental disorders. Neuropsychology
/ original-article
/ Pharmacotherapy
/ Physiological aspects
/ Plasticity (hippocampal)
/ Post-Synaptic Density - ultrastructure
/ postsynaptic density
/ Postsynaptic density proteins
/ Protein kinases
/ Psychiatry
/ Psychology. Psychoanalysis. Psychiatry
/ Psychopathology. Psychiatry
/ Retrovirus
/ Up-Regulation
2013
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GSK-3β overexpression causes reversible alterations on postsynaptic densities and dendritic morphology of hippocampal granule neurons in vivo
by
Hernández, F
, Ávila, J
, Ulloa, F
, Rábano, A
, Llorens-Martín, M
, Jurado-Arjona, J
, Soriano, E
, deFelipe, J
, Teixeira, C M
, Fuster-Matanzo, A
in
631/378/368
/ 692/699/375/365/1283
/ Adult and adolescent clinical studies
/ Alzheimer Disease - enzymology
/ Alzheimer Disease - genetics
/ Alzheimer Disease - physiopathology
/ Alzheimer's disease
/ Animal models
/ Animals
/ Behavioral Sciences
/ Biological and medical sciences
/ Biological Psychology
/ Data processing
/ Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
/ Dendrites - ultrastructure
/ Dendritic branching
/ Enrichment
/ Environment
/ Glycogen
/ Glycogen synthase kinase 3
/ Glycogen Synthase Kinase 3 - biosynthesis
/ Glycogen Synthase Kinase 3 - genetics
/ Glycogen Synthase Kinase 3 beta
/ Granule cells
/ Hippocampal plasticity
/ Hippocampus
/ Hippocampus (Brain)
/ Hippocampus - anatomy & histology
/ Hippocampus - enzymology
/ Hippocampus - physiology
/ Humans
/ Medical sciences
/ Medicine
/ Medicine & Public Health
/ Memory
/ Mice
/ Mice, Transgenic
/ Morphology
/ Neonates
/ Neurodegenerative diseases
/ Neurogenesis
/ Neurogenesis - physiology
/ Neurology
/ Neurons
/ Neurons - cytology
/ Neurons - physiology
/ Neurosciences
/ Organic mental disorders. Neuropsychology
/ original-article
/ Pharmacotherapy
/ Physiological aspects
/ Plasticity (hippocampal)
/ Post-Synaptic Density - ultrastructure
/ postsynaptic density
/ Postsynaptic density proteins
/ Protein kinases
/ Psychiatry
/ Psychology. Psychoanalysis. Psychiatry
/ Psychopathology. Psychiatry
/ Retrovirus
/ Up-Regulation
2013
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GSK-3β overexpression causes reversible alterations on postsynaptic densities and dendritic morphology of hippocampal granule neurons in vivo
Journal Article
GSK-3β overexpression causes reversible alterations on postsynaptic densities and dendritic morphology of hippocampal granule neurons in vivo
2013
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Overview
Adult hippocampal neurogenesis (AHN) is crucial for the maintenance of hippocampal function. Several neurodegenerative diseases such as Alzheimer’s disease (AD) are accompanied by memory deficits that could be related to alterations in AHN. Here, we took advantage of a conditional mouse model to study the involvement of glycogen synthase kinase-3β (GSK-3β) overexpression (OE) in AHN. By injecting GFP- and PSD95-GFP-expressing retroviruses, we have determined that hippocampal GSK-3β-OE causes dramatic alterations in both dendritic tree morphology and post-synaptic densities in newborn neurons. Alterations in previously damaged neurons were reverted by switching off the transgenic system and also by using a physiological approach (environmental enrichment) to increase hippocampal plasticity. Furthermore, comparative morphometric analysis of granule neurons from patients with AD and from GSK-3β overexpressing mice revealed shared morphological alterations. Taken together, these data indicate that GSK-3β is crucial for hippocampal function, thereby supporting this kinase as a relevant target for the treatment of AD.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Adult and adolescent clinical studies
/ Alzheimer Disease - enzymology
/ Alzheimer Disease - genetics
/ Alzheimer Disease - physiopathology
/ Animals
/ Biological and medical sciences
/ Glycogen
/ Glycogen Synthase Kinase 3 - biosynthesis
/ Glycogen Synthase Kinase 3 - genetics
/ Glycogen Synthase Kinase 3 beta
/ Hippocampus - anatomy & histology
/ Humans
/ Medicine
/ Memory
/ Mice
/ Neonates
/ Neurons
/ Organic mental disorders. Neuropsychology
/ Post-Synaptic Density - ultrastructure
/ Postsynaptic density proteins
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