Search Results - "Nerve Degeneration: genetics"

Congenic expression of poly-GA but not poly-PR in mice triggers selective neuron loss and interferon responses found in C9orf72 ALS

Authors: Benedikt Wefers Monika S. Brill Birgit Rathkolb et al.

Contributors: Benedikt Wefers Monika S. Brill Birgit Rathkolb et al.

Source: Acta Neuropathol
Acta neuropathologica 140(2), 121-142 (2020). doi:10.1007/s00401-020-02176-0
Acta Neuropathol. 140, 121–142 (2020)

Subject Terms: 0301 basic medicine, immunology [Nerve Degeneration], genetics [DNA Repeat Expansion], Mice, Transgenic, immunology [Amyotrophic Lateral Sclerosis], Mice, 03 medical and health sciences, Interferon, Amyotrophic Lateral Sclerosis/pathology [MeSH], C9orf72 Protein/genetics [MeSH], Microglia, Nerve Degeneration/immunology [MeSH], Animals [MeSH], DNA Repeat Expansion/genetics [MeSH], Mice, Transgenic [MeSH], Neurodegeneration, Mice [MeSH], FTD, Mouse model, Original Paper, ALS, Interferons/biosynthesis [MeSH], Neurons/pathology [MeSH], Amyotrophic Lateral Sclerosis/genetics [MeSH], Amyotrophic Lateral Sclerosis/immunology [MeSH], Nerve Degeneration/pathology [MeSH], Disease Models, Animal [MeSH], Nerve Degeneration/genetics [MeSH], pathology [Neurons], Animals, ddc:610, pathology [Amyotrophic Lateral Sclerosis], biosynthesis [Interferons], genetics [C9orf72 Protein], Neurons, 0303 health sciences, DNA Repeat Expansion, C9orf72 Protein, Amyotrophic Lateral Sclerosis, pathology [Nerve Degeneration], ddc, 3. Good health, genetics [Amyotrophic Lateral Sclerosis], Disease Models, Animal, genetics [Nerve Degeneration], Nerve Degeneration, C9orf72, Als, Ftd, Mouse Model, Interferons

File Description: application/pdf

Access URL: https://link.springer.com/content/pdf/10.1007/s00401-020-02176-0.pdf
https://pubmed.ncbi.nlm.nih.gov/32562018
https://pubmed.ncbi.nlm.nih.gov/32562018/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7360660
https://www.ncbi.nlm.nih.gov/pubmed/32562018
https://link.springer.com/content/pdf/10.1007/s00401-020-02176-0.pdf
https://mediatum.ub.tum.de/node?id=1619777
https://link.springer.com/article/10.1007/s00401-020-02176-0
https://pub.dzne.de/record/153340
https://resolver.sub.uni-goettingen.de/purl?gro-2/113001
https://rdp.sfb274.de/literature/publications/5
https://push-zb.helmholtz-muenchen.de/frontdoor.php?source_opus=59426
https://repository.publisso.de/resource/frl:6466740
https://epub.ub.uni-muenchen.de/85279/
https://mediatum.ub.tum.de/1578105

Retinal axonal degeneration in Niemann–Pick type C disease

Authors: Tatiana Bremova-Ertl Michael Strupp Marlene Moser et al.

Source: J Neurol
Havla, Joachim; Moser, Marlene; Sztatecsny, Clara; Lotz-Havla, Amelie S; Maier, Esther M; Hizli, Baccara; Schinner, Regina; Kümpfel, Tania; Strupp, Michael; Bremova-Ertl, Tatiana; Schneider, Susanne A (2020). Retinal axonal degeneration in Niemann-Pick type C disease. Journal of neurology, 267(7), pp. 2070-2082. Springer-Medizin-Verlag 10.1007/s00415-020-09796-2 <http://dx.doi.org/10.1007/s00415-020-09796-2>

Subject Terms: Adult, Male, Retinal Ganglion Cells, 0301 basic medicine, Heterozygote, Adolescent, Eye Movements, Heterozygote [MeSH], Aged [MeSH], Retinal Degeneration/pathology [MeSH], Retinal Degeneration/physiopathology [MeSH], Tomography, Optical Coherence [MeSH], Clinical biomarker, Optical coherence tomography, Macula Lutea/pathology [MeSH], Male [MeSH], Niemann-Pick Disease, Type C/diagnostic imaging [MeSH], Child [MeSH], Retinal Degeneration/diagnostic imaging [MeSH], Retinal Ganglion Cells/pathology [MeSH], Axons/ultrastructure [MeSH], Retinal Degeneration/genetics [MeSH], Nerve Degeneration/physiopathology [MeSH], Adolescent [MeSH], Female [MeSH], Adult [MeSH], Humans [MeSH], Nerve Degeneration/diagnostic imaging [MeSH], Niemann-Pick Disease, Type C/pathology [MeSH], Retinal neuroaxonal degeneration, Middle Aged [MeSH], Niemann-Pick Disease, Type C/genetics [MeSH], Intracellular Signaling Peptides and Proteins/genetics [MeSH], Macula Lutea/ultrastructure [MeSH], Eye Movements/physiology [MeSH], Heterozygosity, Retinal Ganglion Cells/ultrastructure [MeSH], Young Adult [MeSH], Eye-Tracking Technology [MeSH], Biomarkers [MeSH], Nerve Degeneration/pathology [MeSH], Axons/pathology [MeSH], Original Communication, Niemann–Pick type C, Nerve Degeneration/genetics [MeSH], Niemann-Pick Disease, Type C/physiopathology [MeSH], 610 Medicine & health, 03 medical and health sciences, 0302 clinical medicine, Niemann-Pick C1 Protein, Humans, Macula Lutea, Child, Eye-Tracking Technology, 10. No inequality, Aged, 2. Zero hunger, Retinal Degeneration, Intracellular Signaling Peptides and Proteins, Niemann-Pick Disease, Type C, Middle Aged, Axons, 3. Good health, Nerve Degeneration, Female, Biomarkers

File Description: application/pdf

Access URL: https://link.springer.com/content/pdf/10.1007/s00415-020-09796-2.pdf
https://pubmed.ncbi.nlm.nih.gov/32222928
https://link.springer.com/article/10.1007/s00415-020-09796-2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7320959
https://europepmc.org/article/PMC/PMC7320959
https://pubmed.ncbi.nlm.nih.gov/32222928/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7320959
https://epub.ub.uni-muenchen.de/73083/
https://boris.unibe.ch/145190/
https://repository.publisso.de/resource/frl:6469676
https://epub.ub.uni-muenchen.de/73083/

Dynactin1 depletion leads to neuromuscular synapse instability and functional abnormalities.

Authors: Bercier, V. Hubbard, J.M. Fidelin, K. et al.

Subject Terms: Amyotrophic Lateral Sclerosis/genetics, Amyotrophic Lateral Sclerosis/metabolism, Animals, Axonal Transport/genetics, Disease Models, Animal, Dynactin Complex/deficiency, Motor Neurons/metabolism, Nerve Degeneration/genetics, Nerve Degeneration/pathology, Neuromuscular Junction/genetics, Spinal Cord/metabolism, Synapses/metabolism, Zebrafish, Amyotrophic lateral sclerosis, Axonal transport, Dynactin1, Neuromuscular junction

File Description: application/pdf

Relation: Molecular Neurodegeneration; https://iris.unil.ch/handle/iris/88310; serval:BIB_17878F9EC16F; 000475673400001

Availability: https://iris.unil.ch/handle/iris/88310
https://doi.org/10.1186/s13024-019-0327-3

Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons.

Authors: Oettinghaus, B. Schulz, J.M. Restelli, L.M. et al.

Subject Terms: Animals, Antioxidants/administration & dosage, Atrophy/genetics, Atrophy/metabolism, Dynamins/biosynthesis, Dynamins/genetics, Hippocampus/growth & development, Hippocampus/metabolism, Memory Disorders/genetics, Memory Disorders/pathology, Mice, Mitochondria/metabolism, Mitochondria/pathology, Mitochondrial Dynamics/genetics, Nerve Degeneration/genetics, Nerve Degeneration/metabolism, Nervous System/growth & development, Nervous System/pathology, Neurons/metabolism, Neurons/pathology, Prosencephalon/growth & development, Prosencephalon/metabolism

File Description: application/pdf

Relation: Cell Death & Differentiation; https://iris.unil.ch/handle/iris/166607; serval:BIB_BDF780D8E819; 000368062000010

Availability: https://iris.unil.ch/handle/iris/166607
https://doi.org/10.1038/cdd.2015.39

Progressive and selective striatal degeneration in primary neuronal cultures using lentiviral vector coding for a mutant huntingtin fragment.

Authors: Zala, D. Benchoua, A. Brouillet, E. et al.

Subject Terms: Animals, Brain-Derived Neurotrophic Factor/pharmacology, Brain-Derived Neurotrophic Factor/therapeutic use, Cell Death/drug effects, Cell Death/genetics, Cells, Cultured, Ciliary Neurotrophic Factor/pharmacology, Ciliary Neurotrophic Factor/therapeutic use, Corpus Striatum/metabolism, Corpus Striatum/physiopathology, Genetic Vectors/genetics, HSP70 Heat-Shock Proteins/metabolism, Humans, Huntington Disease/genetics, Huntington Disease/metabolism, Inclusion Bodies/genetics, Inclusion Bodies/metabolism, Lentivirus/genetics, Microtubule-Associated Proteins/metabolism, Mutation/genetics, Nerve Degeneration/genetics, Nerve Degeneration/metabolism, Nerve Tissue Proteins/genetics, Nerve Tissue Proteins/metabolism, Neurofilament Proteins/metabolism, Neurons/metabolism, Neurons/pathology, Nuclear Proteins/genetics, Nuclear Proteins/metabolism

Relation: Neurobiology of Disease; https://iris.unil.ch/handle/iris/50195; serval:BIB_15371235638A; 000233739100017

Availability: https://iris.unil.ch/handle/iris/50195
https://doi.org/10.1016/j.nbd.2005.05.017

Deregulation of the phosphatidylinositol-3 kinase signaling cascade is associated with neurodegeneration in Npc1-/- mouse brain.

Authors: Bi, Xiaoning Liu, Jihua Yao, Yueqin et al.

Source: The American journal of pathology. 167(4)

Subject Terms: Animals, Biological Markers: metabolism, Blotting, Western, Brain: metabolism, pathology, Brain Chemistry, Cell Nucleus: chemistry, metabolism, Crosses, Genetic, Cytoplasm: chemistry, metabolism, Glycogen Synthase Kinase 3: metabolism, Heterozygote, Homozygote, Immunohistochemistry, Mice, Mice, Inbred BALB C, Mice, Knockout, Models, Biological, NF-kappa B: analysis, chemistry, metabolism, Nerve Degeneration: genetics, metabolism, pathology, Niemann-Pick Diseases: genetics, pathology, Phosphatidylinositol 3-Kinases: metabolism, Phosphorylation, Protein Subunits: metabolism, Proteins: genetics

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Access URL: https://escholarship.org/uc/item/5qc6791h
https://escholarship.org/content/qt5qc6791h/qt5qc6791h.pdf

Mitochondrial DNA Double-Strand Breaks in Oligodendrocytes Cause Demyelination, Axonal Injury, and CNS Inflammation

Authors: Pernille M. Madsen Milena Pinto Shreyans Patel et al.

Source: Madsen, P M, Pinto, M, Patel, S, McCarthy, S, Gao, H, Taherian, M, Karmally, S, Pereira, C V, Dvoriantchikova, G, Ivanov, D, Tanaka, K F, Moraes, C T & Brambilla, R 2017, ' Mitochondrial DNA double-strand breaks in oligodendrocytes cause demyelination, axonal injury, and CNS inflammation ', Journal of Neuroscience, vol. 37, no. 42, pp. 10185-10199 . https://doi.org/10.1523/JNEUROSCI.1378-17.2017

Subject Terms: Central Nervous System, Male, 0301 basic medicine, Encephalomyelitis, Autoimmune, Experimental, Encephalomyelitis, Autoimmune, Experimental/genetics, Demyelinating Diseases/genetics, Mice, Transgenic, Inbred C57BL, Mitochondrial/genetics, DNA, Mitochondrial, Transgenic, DNA, Mitochondrial/genetics, Multiple sclerosis, Double-Stranded, Nerve Degeneration/genetics, Mice, 03 medical and health sciences, Inflammation/genetics, Animals, Animal model, Oxidative phosphorylation, DNA Breaks, Double-Stranded, Experimental/genetics, Encephalomyelitis, Inflammation, DNA Breaks, DNA, Axons, Mitochondria, Oligodendroglia/pathology, Mice, Inbred C57BL, Oligodendroglia, Axons/pathology, Remyelination, Locomotion/physiology, Central Nervous System/pathology, Nerve Degeneration, Female, Demyelination, Locomotion, Autoimmune, Demyelinating Diseases

File Description: application/pdf

Access URL: https://www.jneurosci.org/content/jneuro/37/42/10185.full.pdf
https://pubmed.ncbi.nlm.nih.gov/28931570
https://www.jneurosci.org/content/jneuro/early/2017/09/20/JNEUROSCI.1378-17.2017.full.pdf
https://pubmed.ncbi.nlm.nih.gov/28931570/
http://europepmc.org/articles/PMC5647772
https://keio.pure.elsevier.com/en/publications/mitochondrial-dna-double-strand-breaks-in-oligodendrocytes-cause-
http://www.jneurosci.org/content/early/2017/09/20/JNEUROSCI.1378-17.2017
https://www.jneurosci.org/content/jneuro/37/42/10185.full.pdf
https://findresearcher.sdu.dk:8443/ws/files/137928668/Mitochondrial_DNA_double_strand_breaks_in_oligodendrocytes_cause_demyelination.pdf

Congenic expression of poly-GA but not poly-PR in mice triggers selective neuron loss and interferon responses found in C9orf72 ALS.

Authors: LaClair, Katherine D Zhou, Qihui Wurst, Wolfgang et al.

Source: Acta neuropathologica 140(2), 121 - 142 (2020). doi:10.1007/s00401-020-02176-0

Subject Terms: info:eu-repo/classification/ddc/610, Amyotrophic Lateral Sclerosis: genetics, Amyotrophic Lateral Sclerosis: immunology, Amyotrophic Lateral Sclerosis: pathology, Animals, C9orf72 Protein: genetics, DNA Repeat Expansion: genetics, Disease Models, Animal, Interferons: biosynthesis, Mice, Transgenic, Nerve Degeneration: genetics, Nerve Degeneration: immunology, Nerve Degeneration: pathology, Neurons: pathology

Subject Geographic: DE

Relation: info:eu-repo/semantics/altIdentifier/issn/1432-0533; info:eu-repo/semantics/altIdentifier/pmid/pmid:32562018; info:eu-repo/semantics/altIdentifier/issn/0001-6322; https://pub.dzne.de/record/153340

Availability: https://pub.dzne.de/record/153340
https://pub.dzne.de/search?p=id:%22DZNE-2020-01337%22

Early Neurodegeneration in the Brain of a Child Without Functional PKR-like Endoplasmic Reticulum Kinase

Authors: Bruch, J. Kurz, C. Vasiljevic, A. et al.

Contributors: Bruch, J. Kurz, C. Vasiljevic, A. et al.

Source: Journal of neuropathology and experimental neurology 74(8), 850-857 (2015). doi:10.1097/NEN.0000000000000224

Subject Terms: Male, 0301 basic medicine, Nerve Degeneration/genetics/*pathology, [SDV]Life Sciences [q-bio], eIF-2 Kinase/*deficiency, Fluorescent Antibody Technique, Type 1/genetics/*pathology, Osteochondrodysplasias, deficiency [eIF-2 Kinase], eIF-2 Kinase, 03 medical and health sciences, pathology [Epiphyses], pathology [Brain], Diabetes Mellitus, Humans, ddc:610, Child, Preschool, 0303 health sciences, EIF2AK3 protein, human, pathology [Diabetes Mellitus, Type 1], pathology [Nerve Degeneration], Brain, Immunohistochemistry, genetics [Diabetes Mellitus, Type 1], abnormalities [Epiphyses], genetics [Osteochondrodysplasias], 3. Good health, [SDV] Life Sciences [q-bio], Osteochondrodysplasias/genetics/*pathology, Diabetes Mellitus, Type 1, genetics [Nerve Degeneration], Child, Preschool, Nerve Degeneration, pathology [Osteochondrodysplasias], Epiphyses/*abnormalities/pathology, Epiphyses, Brain/*pathology

Access URL: https://academic.oup.com/jnen/article-pdf/74/8/850/9564059/74-8-850.pdf
https://pubmed.ncbi.nlm.nih.gov/26172286
https://mediatum.ub.tum.de/1322418
https://pubmed.ncbi.nlm.nih.gov/26172286/
https://doi.org/10.1097%2FNEN.0000000000000224
https://academic.oup.com/jnen/article/74/8/850/2917725
https://www.ncbi.nlm.nih.gov/pubmed/26172286

HIF-1α is a protective factor in conditional PHD2-deficient mice suffering from severe HIF-2α–induced excessive erythropoiesis

Authors: Joanna Kalucka Guo-Hua Fong Teresa Otto et al.

Contributors: Joanna Kalucka Guo-Hua Fong Teresa Otto et al.

Source: Franke, K, Kalucka, J, Mamlouk, S, Singh, R P, Muschter, A, Weidemann, A, Iyengar, V, Jahn, S, Wieczorek, K, Geiger, K, Muders, M, Sykes, A M, Poitz, D M, Ripich, T, Otto, T, Bergmann, S, Breier, G, Baretton, G, Fong, G-H, Greaves, D R, Bornstein, S, Chavakis, T, Fandrey, J, Gassmann, M & Wielockx, B 2013, 'HIF-1α is a protective factor in conditional PHD2-deficient mice suffering from severe HIF-2α-induced excessive erythropoiesis', Blood, vol. 121, no. 8, pp. 1436-45. https://doi.org/10.1182/blood-2012-08-449181
BLOOD

Subject Terms: Keratinocytes, Male, 0301 basic medicine, 1303 Biochemistry, 2720 Hematology, Medizin, nerve degeneration, Kidney, Severity of Illness Index, 1307 Cell Biology, Nerve Degeneration/genetics, Mice, Basic Helix-Loop-Helix Transcription Factors, Cells, Cultured, Mice, Knockout, heart sound p2, 0303 health sciences, Polycythemia/genetics, Hematopoiesis, Extramedullary/physiology, Brain, Kidney/cytology, 10081 Institute of Veterinary Physiology, Hematopoiesis, Extramedullary, Thrombocytopenia/genetics, Female, Hypoxia-Inducible Factor 1, alpha Subunit/genetics, kidney, mice, Procollagen-Proline Dioxygenase, 610 Medicine & health, Polycythemia, Brain/physiology, Hypoxia-Inducible Factor-Proline Dioxygenases, 03 medical and health sciences, Procollagen-Proline Dioxygenase/genetics, 11554 Zurich Center for Integrative Human Physiology (ZIHP), protective factors, Animals, Humans, Erythropoietin, 2403 Immunology, Basic Helix-Loop-Helix Transcription Factors/genetics, Keratinocytes/cytology, Erythropoietin/genetics, Fibroblasts, Hypoxia-Inducible Factor 1, alpha Subunit, Erythrocytosis, Mice, Inbred C57BL, Fibroblasts/cytology, Nerve Degeneration, 570 Life sciences, biology, erythropoiesis

File Description: Franke_Blood_2012.pdf - application/pdf

Access URL: https://europepmc.org/articles/pmc3628111
https://pubmed.ncbi.nlm.nih.gov/23264599
https://www.zora.uzh.ch/id/eprint/71026/
https://pubmed.ncbi.nlm.nih.gov/23264599/
https://www.sciencedirect.com/science/article/pii/S0006497120420877
http://europepmc.org/articles/PMC3628111
http://www.bloodjournal.org/content/early/2012/12/20/blood-2012-08-449181
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628111/
https://ora.ox.ac.uk/objects/uuid:eb1c37c4-8099-4c81-bd1c-04cb10f4cd8d
https://doi.org/10.1182/blood-2012-08-449181
https://hdl.handle.net/20.500.12866/10391
https://doi.org/10.1182/blood-2012-08-449181
https://www.zora.uzh.ch/id/eprint/71026/
https://doi.org/10.5167/uzh-71026
https://pure.au.dk/portal/en/publications/1d56ffc9-cfd6-4cb1-9d17-02fa78443aa0
https://doi.org/10.1182/blood-2012-08-449181
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628111/
https://www.ncbi.nlm.nih.gov/pubmed/23264599
https://doi.org/10.1182/blood-2012-08-449181

Vector-Mediated Delivery of bcl-2 Prevents Degeneration of Auditory Hair Cells and Neurons after Injury

Authors: Staecker, Hinrich Liu, Wei Malgrange, Brigitte et al.

Source: ORL. 69:43-50

Subject Terms: 0301 basic medicine, Cell Survival, Genes, bcl-2/physiology, Genetic Vectors, Brain-Derived Neurotrophic Factor/pharmacology, Apoptosis, Biochimie, biophysique & biologie moléculaire, Neomycin/toxicity, Adenoviridae, Nerve Degeneration/genetics, 03 medical and health sciences, Neurons/drug effects/pathology, Spiral Ganglion/drug effects/pathology, Apoptosis/genetics, Hair Cells, Auditory, Animals, Simplexvirus, Rats, Wistar, Membrane Potential, Mitochondrial/drug effects/genetics, Cells, Cultured, Membrane Potential, Mitochondrial, Neurons, 2. Zero hunger, 0303 health sciences, Brain-Derived Neurotrophic Factor, Hair Cells, Auditory/drug effects/pathology, Neomycin, Life sciences, Genes, bcl-2, Rats, 3. Good health, Oxidative Stress, Animals, Newborn, Nerve Degeneration, Sciences du vivant, Cisplatin, Spiral Ganglion, Cisplatin/toxicity, Biochemistry, biophysics & molecular biology

Access URL: https://pubmed.ncbi.nlm.nih.gov/17085952
https://orbi.uliege.be/handle/2268/29437
https://miami.pure.elsevier.com/en/publications/vector-mediated-delivery-of-bcl-2-prevents-degeneration-of-audito
https://europepmc.org/article/MED/17085952
https://www.ncbi.nlm.nih.gov/pubmed/17085952

Cell death pathways differ in several mouse models with motoneurone disease: analysis of pure motoneurone populations at a presymptomatic age

Authors: Perrin, Florence E Boisset, Gaëlle Lathuiliere, Aurélien et al.

Contributors: Perrin, Florence E Boisset, Gaëlle Lathuiliere, Aurélien et al.

Source: Journal of neurochemistry, Vol. 98, No 6 (2006) pp. 1959-1972

Subject Terms: 0301 basic medicine, Spinal Cord / pathology, Cytoplasm, 616.8, RNA, Messenger / metabolism, Motor Neuron Disease / physiopathology, Nerve Degeneration / pathology, Gene Expression, Cell Separation, Polymerase Chain Reaction, Motor Neurons / metabolism, Mice, Mice, Neurologic Mutants, 03 medical and health sciences, Computer Systems, Cytoplasm / metabolism, Vimentin / metabolism, Animals, Vimentin / genetics, Motor Neuron Disease, Oligonucleotide Array Sequence Analysis, Inclusion Bodies, Motor Neurons, 0303 health sciences, Motor Neuron Disease / genetics, Cell Death, Gene Expression Profiling, Lasers, [SCCO.NEUR] Cognitive science/Neuroscience, Nerve Degeneration / physiopathology, ddc:616.8, Cell Separation / methods, Disease Models, Animal, Animals, Newborn, Gene Expression Regulation, Nerve Degeneration, Disease Progression, Inclusion Bodies / pathology, Microdissection, Nerve Degeneration / genetics, Motor Neuron Disease / pathology

File Description: application/pdf

Access URL: https://pubmed.ncbi.nlm.nih.gov/16831193
https://hal.science/hal-02156303v1
https://doi.org/10.1111/j.1471-4159.2006.04024.x
https://hal.archives-ouvertes.fr/hal-02156303
https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1471-4159.2006.04024.x
https://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2006.04024.x
https://pubmed.ncbi.nlm.nih.gov/16831193/
https://europepmc.org/abstract/MED/16831193
http://europepmc.org/abstract/MED/16831193
https://archive-ouverte.unige.ch/unige:155325

Gene expression profiling in frataxin deficient mice: Microarray evidence for significant expression changes without detectable neurodegeneration

Authors: Giovanni Coppola Dmitri Tentler Manuela M. Santos et al.

Source: Neurobiology of Disease, Vol 22, Iss 2, Pp 302-311 (2006)

Subject Terms: Central Nervous System, Male, 0301 basic medicine, Iron-Binding Proteins -- genetics, Microarray, Knockin/knockout, Mice, Mitochondria -- metabolism, Iron-Binding Proteins, Spinal Cord -- pathology, Mutation -- genetics, Nerve Degeneration -- genetics, Oligonucleotide Array Sequence Analysis, Mice, Knockout, 0303 health sciences, Frataxin, Nerve Degeneration -- physiopathology, Genetic Predisposition to Disease -- genetics, Sciences bio-médicales et agricoles, Central Nervous System -- pathology, Friedreich Ataxia -- metabolism, Mitochondria, Phenotype, Spinal Cord, Friedreich Ataxia -- genetics, Female, Central Nervous System -- metabolism, RC321-571, Knockout, Spinal Cord -- metabolism, Spinal Cord -- physiopathology, Neurosciences. Biological psychiatry. Neuropsychiatry, Mouse model, Cell Line, Central Nervous System -- physiopathology, 03 medical and health sciences, Animals, Humans, Genetic Predisposition to Disease, Gene Expression Regulation -- genetics, Neurodegeneration, Friedreich Ataxia -- physiopathology, Animal, Mitochondria -- genetics, Gene Expression Profiling, Friedreich's ataxia, Disease Models, Animal, Gene Expression Regulation, Friedreich Ataxia, Nerve Degeneration -- metabolism, Disease Models, Mutation, Nerve Degeneration

File Description: 1 full-text file(s): application/pdf

Access URL: https://europepmc.org/articles/pmc2886035?pdf=render
https://pubmed.ncbi.nlm.nih.gov/16442805
https://doaj.org/article/1a7968552aa14ccc96b1b5c347a4e4e9
https://www.sciencedirect.com/science/article/pii/S096999610500313X
https://core.ac.uk/display/8851298
https://doaj.org/article/1a7968552aa14ccc96b1b5c347a4e4e9
https://difusion.ulb.ac.be/vufind/Record/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/51409/Details
https://koreauniv.pure.elsevier.com/en/publications/gene-expression-profiling-in-frataxin-deficient-mice-microarray-e
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886035

Early nuclear translocation of endonuclease G and subsequent DNA fragmentation after transient focal cerebral ischemia in mice

Authors: Gyung Whan Kim Kyoung Ja Cho Byung I. Lee et al.

Contributors: Gyung Whan Kim Kyoung Ja Cho Byung I. Lee et al.

Source: Neuroscience Letters. 386:23-27

Subject Terms: Cell Nucleus/physiology, Male, 0301 basic medicine, Time Factors, Cerebral Infarction/metabolism, Nerve Degeneration/physiopathology, Endonuclease G, Active Transport, Cell Nucleus, Fluorescent Antibody Technique, DNA fragmentation, DNA Fragmentation, Nerve Degeneration/metabolism, Transient/genetics, Transient focal cerebral ischemia, Nerve Degeneration/genetics, Mice, 03 medical and health sciences, Transient/metabolism, Mitochondria/metabolism, Animals, Cell Nucleus, 0303 health sciences, Endodeoxyribonucleases, Brain/physiopathology, Flavoproteins, Animal, Ischemic Attack, Apoptosis Inducing Factor, Brain, Membrane Proteins, Cerebral Infarction, Brain/metabolism, Active Transport, Mitochondria, Endodeoxyribonucleases/metabolism, Cell Nucleus/metabolism, Disease Models, Animal, Ischemic Attack, Transient, Disease Models, Flavoproteins/metabolism, Nerve Degeneration, DNA Fragmentation/physiology, Membrane Proteins/metabolism, Transient/physiopathology, Cerebral Infarction/physiopathology

Access URL: https://pubmed.ncbi.nlm.nih.gov/15979239
https://www.sciencedirect.com/science/article/pii/S030439400500621X
https://www.ncbi.nlm.nih.gov/pubmed/15979239
https://pubmed.ncbi.nlm.nih.gov/15979239/

Endothelial Cell-specific Over-expression of Endothelin- 1 Leads to More Severe Cerebral Damage following Transient Middle Cerebral Artery Occlusion

Authors: Ho, MCY Leung, JWC Chung, SK et al.

Source: Journal of Cardiovascular Pharmacology. 44:S293-S300

Subject Terms: Male, Infarct, Neurological deficit, Mice, Transgenic, Rna, Messenger - Metabolism, Hippocampus, Severity of Illness Index, Transgenic, Endothelium, Vascular - Metabolism - Pathology, Mice, 03 medical and health sciences, 0302 clinical medicine, Transgenic mice, Brain - Blood Supply - Pathology, Animals, Endothelium, RNA, Messenger, Infarction, Middle Cerebral Artery - Genetics - Metabolism - Pathology, In Situ Hybridization, Cell Death, Endothelin-1, Animal, Reverse Transcriptase Polymerase Chain Reaction, Middle Cerebral Artery - Genetics - Metabolism - Pathology, Brain, Endothelin-1 - Genetics - Metabolism, Infarction, Middle Cerebral Artery, Hippocampus - Blood Supply - Pathology, Immunohistochemistry, Up-Regulation, 3. Good health, Stroke, Severity Of Illness Index, Disease Models, Animal, Infarction, Disease Models, Nerve Degeneration, Rna, Endothelium, Vascular, Vascular - Metabolism - Pathology, Messenger - Metabolism, Nerve Degeneration - Genetics - Metabolism - Pathology

Access URL: https://pubmed.ncbi.nlm.nih.gov/15838304
http://hub.hku.hk/handle/10722/146628
https://pubmed.ncbi.nlm.nih.gov/15838304/
https://www.ncbi.nlm.nih.gov/pubmed/15838304
https://core.ac.uk/display/37967936
http://hdl.handle.net/10722/146628

No alterations of hippocampal neuronal number and synaptic bouton number in a transgenic mouse model expressing the β-cleaved C-terminal APP fragment

Authors: Oliver Wirths Christoph Schmitz Wilma D.J. van de Berg et al.

Source: Neurobiology of Disease, Vol 12, Iss 2, Pp 110-120 (2003)
Rutten, B P F, Wirths, O, Van de Berg, W D J, Lichtenthaler, S F, Vehoff, J, Steinbusch, H W M, Korr, H, Beyreuther, K, Multhaup, G, Bayer, T A & Schmitz, C 2003, 'No alterations of hippocampal neuronal number and synaptic bouton number in a transgenic mouse model expressing the beta-cleaved C-terminal APP fragment', Neurobiology of Disease, vol. 12, no. 2, pp. 110-20.

Subject Terms: 0301 basic medicine, Protein Structure, Mutation/genetics, Transgenes/genetics, Amyloid beta-Peptides/biosynthesis, Stereology, Hippocampus/metabolism, Presynaptic Terminals, Synaptophysin, Neurosciences. Biological psychiatry. Neuropsychiatry, Mice, Transgenic, Synaptophysin/metabolism, Cell Death/genetics, Tertiary/genetics, Gene Expression Regulation/genetics, Hippocampus, Transgenic, Nerve Degeneration/genetics, Amyloid beta-Protein Precursor, Mice, 03 medical and health sciences, Alzheimer Disease, SPA4CT, Animals, Transgenes, Peptide Fragments/genetics, Neurodegeneration, Alzheimer Disease/genetics, 0303 health sciences, Amyloid beta-Peptides, Cell Death, Animal, Intraneuronal Aβ, Amyloid beta-Protein Precursor/metabolism, Immunohistochemistry, Peptide Fragments, Protein Structure, Tertiary, 3. Good health, Presynaptic Terminals/metabolism, Disease Models, Animal, Gene Expression Regulation, Disease Models, Mutation, Nerve Degeneration, RC321-571

Access URL: https://pubmed.ncbi.nlm.nih.gov/12667466
https://doaj.org/article/ca01e9fa4854444c9a81e90af2847475
https://europepmc.org/article/med/12667466
http://www.ncbi.nlm.nih.gov/pubmed/12667466
http://www.sciencedirect.com/science/article/pii/S0969996102000153
https://www.sciencedirect.com/science/article/pii/S0969996102000153
https://research.vumc.nl/en/publications/no-alterations-of-hippocampal-neuronal-number-and-synaptic-bouton
https://www.narcis.nl/publication/RecordID/oai%3Apure.atira.dk%3Apublications%2Fe55e01ca-ad59-4065-ab12-36f8ab98683f
https://research.vumc.nl/en/publications/e55e01ca-ad59-4065-ab12-36f8ab98683f
https://pure.amsterdamumc.nl/en/publications/fe653070-42d8-408d-9ce4-edccbc7badbd

'New' functions for 'old' proteins: The role of the calcium-binding proteins calbindin D-28k, calretinin and parvalbumin, in cerebellar physiology. Studies with knockout mice

Authors: Beat Schwaller Serge N. Schiffmann Michael Meyer

Source: The Cerebellum. 1:241-258

Subject Terms: 0301 basic medicine, Homeostasis -- physiology, Cerebellar Ataxia -- genetics, Cerebellum -- cytology, Cerebellar Ataxia, Knockout, Inbred Strains, Mice, Inbred Strains, Motor Activity, Synaptic plasticity, Mice, 03 medical and health sciences, S100 Calcium Binding Protein G, Cerebellum -- physiology, Motor Activity -- physiology, Cerebellum, Animals, Homeostasis, Motor Activity -- genetics, Calcium-Binding Protein, Nerve Degeneration -- genetics, Mice, Knockout, 0303 health sciences, Cerebellum -- metabolism, Sciences bio-médicales et agricoles, Parvalbumins, Vitamin D-Dependent -- metabolism, Purkinje cells, Calbindin 2, Mutation, Nerve Degeneration, Calcium -- metabolism, Cerebellar Ataxia -- physiopathology, Ataxia, Calcium, Parvalbumins -- metabolism, Knockout mice

File Description: No full-text files

Access URL: https://pubmed.ncbi.nlm.nih.gov/12879963
https://europepmc.org/article/MED/12879963
https://difusion.ulb.ac.be/vufind/Record/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/51810/Details
https://www.ncbi.nlm.nih.gov/pubmed/12879963
https://core.ac.uk/display/8851686
https://link.springer.com/10.1080/147342202320883551

CAG repeats determine brain atrophy in spinocerebellar ataxia 17: a VBM study

Authors: Reetz, K. Kleinman, A. Klein, C. et al.

Source: PLoS one 6, e15125 (2011). doi:10.1371/journal.pone.0015125

Subject Terms: info:eu-repo/classification/ddc/500, Adult, Age of Onset, Atrophy: genetics, Atrophy: metabolism, Brain: pathology, Case-Control Studies, Cerebellum: pathology, Disease Progression, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Nerve Degeneration: genetics, Spinocerebellar Ataxias: genetics, Spinocerebellar Ataxias: pathology, Trinucleotide Repeats

Subject Geographic: DE

Relation: info:eu-repo/semantics/altIdentifier/hdl/2128/11174; info:eu-repo/semantics/altIdentifier/pmid/pmid:21311576; info:eu-repo/semantics/altIdentifier/wos/WOS:000286520600008; info:eu-repo/semantics/altIdentifier/issn/1932-6203

Availability: https://juser.fz-juelich.de/record/20071
https://juser.fz-juelich.de/search?p=id:%22PreJuSER-20071%22

The oral antidiabetic pioglitazone protects from neurodegeneration and amyotrophic lateral sclerosis-like symptoms in superoxide dismutase-G93A transgenic mice.

Authors: Schütz, Burkhard Reimann, Jens Dumitrescu-Ozimek, Lucia et al.

Source: Journal of Neuroscience, 25 (34), 7805 - 7812 (2005-08-24)

Subject Terms: Hypoglycemic Agents, Neuroprotective Agents, Thiazolidinediones, SOD1 G93A protein, Superoxide Dismutase, Pioglitazone, Administration, Oral, Amyotrophic Lateral Sclerosis/genetics, Amyotrophic Lateral Sclerosis/pathology, Amyotrophic Lateral Sclerosis/prevention & control, Animals, Humans, Hypoglycemic Agents/administration & dosage, Male, Mice, Inbred C57BL, Transgenic, Nerve Degeneration/genetics, Nerve Degeneration/pathology, Nerve Degeneration/prevention & control, Neuroprotective Agents/administration & dosage, Superoxide Dismutase/biosynthesis, Superoxide Dismutase/genetics, Thiazolidinediones/administration & dosage, Degeneration, Glia, Microglia, Motor neurons, Neuroinflammation

Relation: urn:issn:0270-6474; urn:issn:1529-2401; https://orbilu.uni.lu/handle/10993/60986; info:hdl:10993/60986; https://orbilu.uni.lu/bitstream/10993/60986/1/7805.full.pdf; info:pmid:16120782; wos:000231439300012

Availability: https://orbilu.uni.lu/handle/10993/60986
https://orbilu.uni.lu/bitstream/10993/60986/1/7805.full.pdf
https://doi.org/10.1523/JNEUROSCI.2038-05.2005

Identification of 2 Loci at Chromosomes 9 and 14 in a Multiplex Family With Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis

Authors: Gijselinck, Ilse Engelborghs, Sebastiaan Maes, Githa et al.

Contributors: Gijselinck, Ilse Engelborghs, Sebastiaan Maes, Githa et al.

Source: Archives of neurology

Subject Terms: Male, 0301 basic medicine, Genetic Linkage, DNA Mutational Analysis, Chromosomes, Human, Pair 9/genetics, Nerve Degeneration/genetics, 03 medical and health sciences, Fatal Outcome, 0302 clinical medicine, Belgium, Chromosomes, Human, Pair 14/genetics, Brain/metabolism, Humans, Genetic Predisposition to Disease, Genetic Testing, Aged, Genetic Linkage/genetics, Chromosomes, Human, Pair 14, Genetic Predisposition to Disease/genetics, Neurons/pathology, Amyotrophic Lateral Sclerosis, Brain, Chromosome Mapping, Amyotrophic Lateral Sclerosis/genetics, Middle Aged, 3. Good health, Haplotypes, Nerve Degeneration, Female, Frontotemporal Lobar Degeneration/genetics, Human medicine, Frontotemporal Lobar Degeneration, Chromosomes, Human, Pair 9, Genome-Wide Association Study

Access URL: https://pubmed.ncbi.nlm.nih.gov/20457961
https://jamanetwork.com/journals/jamaneurology/fullarticle/800160
https://www.ncbi.nlm.nih.gov/pubmed/20457961
https://archneur.jamanetwork.com/article.aspx?articleid=800160
https://hdl.handle.net/10067/826700151162165141
https://hdl.handle.net/20.500.14017/b1582af0-6f6f-4c4f-b12c-515898c477fe
https://doi.org/10.1001/archneurol.2010.82
https://biblio.vub.ac.be/vubir/identification-of-2-loci-at-chromosomes-9-and-14-in-a-multiplex-family-with-frontotemporal-lobar-degeneration-and-amyotrophic-lateral-sclerosis(b1582af0-6f6f-4c4f-b12c-515898c477fe).html