[1]
|
Crome, L. and Erdohazi, M. (1966) Main Pathological Findings in Hydrocephalic Children Treated by VentriculoAtrial Shunt. Archives of Disease in Childhood, 41, 179-182. http://dx.doi.org/10.1136/adc.41.216.179
|
[2]
|
Jernigan, T.L., et al., (1993) Cerebral Morphologic Distinctions between Williams and Down Syndromes. Archives of Neurology, 50, 186-191. http://dx.doi.org/10.1001/archneur.1993.00540020062019
|
[3]
|
Coyle, J.T., Oster-Granite, M.L., and Gearhart, J.D. (1986) The Neurobiologic Consequences of Down Syndrome. Brain Research Bulletin, 16, 773-787. http://dx.doi.org/10.1016/0361-9230(86)90074-2
|
[4]
|
Griffin, W.S., et al., (1989) Brain Interleukin 1 and S-100 Immunoreactivity Are Elevated in Down Syndrome and Alzheimer Disease. Proceedings of the National Academy of Sciences of the United States of America, 86, 7611-7615. http://dx.doi.org/10.1073/pnas.86.19.7611
|
[5]
|
Rumble, B., et al., (1989) Amyloid A4 Protein and Its Precursor in Down Syndrome and Alzheimer’s Disease. The New England Journal of Medicine, 320, 1446-1452. http://dx.doi.org/10.1056/NEJM198906013202203
|
[6]
|
Sabbagh, M.N., et al., (2011) Positron Emission Tomography and Neuropathologic Estimates of Fibrillar AmyloidBeta in a Patient with Down Syndrome and Alzheimer Disease. Archives of Neurology, 68, 1461-1466. http://dx.doi.org/10.1001/archneurol.2011.535
|
[7]
|
Braudeau, J., et al., (2011) Chronic Treatment with a Promnesiant GABA-A α5-Selective Inverse Agonist Increases Immediate Early Genes Expression during Memory Processing in Mice and Rectifies Their Expression Levels in a Down Syndrome Mouse Model. Advances in Pharmacological Sciences, 2011, Article ID: 153218.
|
[8]
|
Das, I. and Reeves, R.H. (2011) The Use of Mouse Models to Understand and Improve Cognitive Deficits in Down Syndrome. Disease Models & Mechanisms, 4, 596-606. http://dx.doi.org/10.1242/dmm.007716
|
[9]
|
De la Torre, R., et al., (2013) Epigallocatechin-3-gallate, a DYRK1A Inhibitor, Rescues Cognitive Deficits in Down Syndrome Mouse Models and in Humans. Molecular Nutrition & Food Research, 58, 278-288.
|
[10]
|
Jiang, J., et al., (2013) Translating Dosage Compensation to Trisomy 21. Nature, 500, 296-300. http://dx.doi.org/10.1038/nature12394
|
[11]
|
Herault, Y., et al., (2012) The in Vivo Down Syndrome Genomic Library in Mouse. Progress in Brain Research, 197, 169-197. http://dx.doi.org/10.1016/B978-0-444-54299-1.00009-1
|
[12]
|
Rueda, N., Florez, J. and Martinez-Cue, C. (2012) Mouse Models of Down Syndrome as a Tool to Unravel the Causes of Mental Disabilities. Neural Plasticity, 2012, Article ID: 584071.
|
[13]
|
Davisson, M.T., Schmidt, C. and Akeson, E.C. (1990) Segmental Trisomy of Murine Chromosome 16: A New Model System for Studying Down Syndrome. Progress in Clinical and Biological Research, 360, 263-280.
|
[14]
|
Davisson, M.T., et al., (1993) Segmental Trisomy as a Mouse Model for Down Syndrome. Progress in Clinical and Biological Research, 384, 117-133.
|
[15]
|
Reeves, R.H., et al., (1995) A Mouse Model for Down Syndrome Exhibits Learning and Behaviour Deficits. Nature Genetics, 11, 177-184. http://dx.doi.org/10.1038/ng1095-177
|
[16]
|
Li, Z., et al. (2007) Duplication of the Entire 22.9 Mb Human Chromosome 21 Syntenic Region on Mouse Chromosome 16 Causes Cardiovascular and Gastrointestinal Abnormalities. Human Molecular Genetics, 16, 1359-1366. http://dx.doi.org/10.1093/hmg/ddm086
|
[17]
|
O’Doherty, A., et al. (2005) An Aneuploid Mouse Strain Carrying Human Chromosome 21 with Down Syndrome Phenotypes. Science, 309, 2033-2037. http://dx.doi.org/10.1126/science.1114535
|
[18]
|
Olson, L.E., et al. (2007) Trisomy for the Down Syndrome “Critical Region” Is Necessary but Not Sufficient for Brain Phenotypes of Trisomic Mice. Human Molecular Genetics, 16, 774-782. http://dx.doi.org/10.1093/hmg/ddm022
|
[19]
|
Pereira, P.L., et al. (2009) A New Mouse Model for the Trisomy of the Abcg1-U2af1 Region Reveals the Complexity of the Combinatorial Genetic Code of Down Syndrome. Human Molecular Genetics, 18, 4756-4769. http://dx.doi.org/10.1093/hmg/ddp438
|
[20]
|
Yu, T., et al. (2010) A Mouse Model of Down Syndrome Trisomic for All Human Chromosome 21 Syntenic Regions. Human Molecular Genetics, 19, 2780-2791. http://dx.doi.org/10.1093/hmg/ddq179
|
[21]
|
Holtzman, D.M., et al. (1996) Developmental Abnormalities and Age-Related Neurodegeneration in a Mouse Model of Down Syndrome. Proceedings of the National Academy of Sciences of the United States of America, 93, 13333-13338. http://dx.doi.org/10.1073/pnas.93.23.13333
|
[22]
|
Dierssen, M., Herault, Y. and Estivill, X. (2009) Aneuploidy: From a Physiological Mechanism of Variance to Down Syndrome. Physiological Reviews, 89, 887-920. http://dx.doi.org/10.1152/physrev.00032.2007
|
[23]
|
Aldridge, K., et al. (2007) Differential Effects of Trisomy on Brain Shape and Volume in Related Aneuploid Mouse Models. American Journal of Medical Genetics Part A, 143A, 1060-1070. http://dx.doi.org/10.1002/ajmg.a.31721
|
[24]
|
Belichenko, P.V., et al. (2004) Synaptic Structural Abnormalities in the Ts65Dn Mouse Model of Down Syndrome. Journal of Comparative Neurology, 480, 281-298. http://dx.doi.org/10.1002/cne.20337
|
[25]
|
Best, T.K., Siarey, R.J. and Galdzicki, Z. (2007) Ts65Dn, a Mouse Model of Down Syndrome, Exhibits Increased GABAB-Induced Potassium Current. Journal of Neurophysiology, 97, 892-900. http://dx.doi.org/10.1152/jn.00626.2006
|
[26]
|
Contestabile, A., et al. (2007) Cell Cycle Alteration and Decreased Cell Proliferation in the Hippocampal Dentate Gyrus and in the Neocortical Germinal Matrix of Fetuses with Down Syndrome and in Ts65Dn Mice. Hippocampus, 17, 665-678. http://dx.doi.org/10.1002/hipo.20308
|
[27]
|
Dierssen, M., et al. (2003) Alterations of Neocortical Pyramidal Cell Phenotype in the Ts65Dn Mouse Model of Down Syndrome: Effects of Environmental Enrichment. Cerebral Cortex, 13, 758-764. http://dx.doi.org/10.1093/cercor/13.7.758
|
[28]
|
Escorihuela, R.M., et al. (1995) A Behavioral Assessment of Ts65Dn Mice: A Putative Down Syndrome Model. Neuroscience Letters, 199, 143-146. http://dx.doi.org/10.1016/0304-3940(95)12052-6
|
[29]
|
Escorihuela, R.M., et al. (1998) Impaired Shortand Long-Term Memory in Ts65Dn Mice, a Model for Down Syndrome. Neuroscience Letters, 247, 171-174. http://dx.doi.org/10.1016/S0304-3940(98)00317-6
|
[30]
|
Hanson, J.E., et al. (2007) The Functional Nature of Synaptic Circuitry Is Altered in Area CA3 of the Hippocampus in a Mouse Model of Down’s Syndrome. The Journal of Physiology, 579, 53-67. http://dx.doi.org/10.1113/jphysiol.2006.114868
|
[31]
|
Insausti, A.M., et al. (1998) Hippocampal Volume and Neuronal Number in Ts65Dn Mice: A Murine Model of Down Syndrome. Neuroscience Letters, 253, 175-178. http://dx.doi.org/10.1016/S0304-3940(98)00641-7
|
[32]
|
Kurt, M.A., et al. (2000) Synaptic Deficit in the Temporal Cortex of Partial Trisomy 16 (Ts65Dn) Mice. Brain Research, 858, 191-197. http://dx.doi.org/10.1016/S0006-8993(00)01984-3
|
[33]
|
Siarey, R.J., et al. (2006) Altered Signaling Pathways Underlying Abnormal Hippocampal Synaptic Plasticity in the Ts65Dn Mouse Model of Down Syndrome. Journal of Neurochemistry, 98, 1266-1277. http://dx.doi.org/10.1111/j.1471-4159.2006.03971.x
|
[34]
|
Seo, H. and Isacson, O. (2005) Abnormal APP, Cholinergic and Cognitive Function in Ts65Dn Down’s Model Mice. Experimental Neurology, 193, 469-480. http://dx.doi.org/10.1016/j.expneurol.2004.11.017
|
[35]
|
Ruparelia, A., Pearn, M.L. and Mobley, W.C. (2012) Cognitive and Pharmacological Insights from the Ts65Dn Mouse Model of Down Syndrome. Current Opinion in Neurobiology, 22, 880-886. http://dx.doi.org/10.1016/j.conb.2012.05.002
|
[36]
|
Denic, A., et al. (2011) MRI in Rodent Models of Brain Disorders. Neurotherapeutics, 8, 3-18. http://dx.doi.org/10.1007/s13311-010-0002-4
|
[37]
|
Meme, S., et al. (2009) MRI Characterization of Structural Mouse Brain Changes in Response to Chronic Exposure to the Glufosinate Ammonium Herbicide. Toxicological Sciences, 111, 321-330. http://dx.doi.org/10.1093/toxsci/kfp174
|
[38]
|
Herlidou, S., et al. (1999) Comparison of Automated and Visual Texture Analysis in MRI: Characterization of Normal and Diseased Skeletal Muscle. Magnetic Resonance Imaging, 17, 1393-1397. http://dx.doi.org/10.1016/S0730-725X(99)00066-1
|
[39]
|
Julesz, B., et al. (1973) Inability of Humans to Discriminate between Visual Textures That Agree in Second-Order Statistics-Revisited. Perception, 2, 391-405. http://dx.doi.org/10.1068/p020391
|
[40]
|
Calas, A.G., et al. (2008) Chronic Exposure to Glufosinate-Ammonium Induces Spatial Memory Impairments, Hippocampal MRI Modifications and Glutamine Synthetase Activation in Mice. Neurotoxicology, 29, 740-747. http://dx.doi.org/10.1016/j.neuro.2008.04.020
|
[41]
|
Conners, R.W. and Harlow, C.A. (1980) A Theoretical Comparison of Texture Algorithms. IEEE Transactions on Pattern Analysis and Machine Intelligence, 2, 204-222. http://dx.doi.org/10.1109/TPAMI.1980.4767008
|
[42]
|
Jirak, D., et al. (2002) Texture Analysis of Human Liver. Journal of Magnetic Resonance Imaging, 15, 68-74. http://dx.doi.org/10.1002/jmri.10042
|
[43]
|
Herlidou, S., et al. (2004) Influence of Age and Osteoporosis on Calcaneus Trabecular Bone Structure: A Preliminary in Vivo MRI Study by Quantitative Texture Analysis. Magnetic Resonance Imaging, 22, 237-343. http://dx.doi.org/10.1016/j.mri.2003.07.007
|
[44]
|
Herlidou-Meme, S., et al. (2003) MRI Texture Analysis on Texture Test Objects, Normal Brain and Intracranial Tumors. Magnetic Resonance Imaging, 21, 989-993. http://dx.doi.org/10.1016/S0730-725X(03)00212-1
|
[45]
|
Baxter, L.L., et al. (2000) Discovery and Genetic Localization of Down Syndrome Cerebellar Phenotypes Using the Ts65Dn Mouse. Human Molecular Genetics, 9, 195-202. http://dx.doi.org/10.1093/hmg/9.2.195
|
[46]
|
Sebrie, C., et al. (2008) Increased Dosage of DYRK1A and Brain Volumetric Alterations in a YAC Model of Partial Trisomy 21. The Anatomical Record, 291, 254-262. http://dx.doi.org/10.1002/ar.20640
|
[47]
|
Chen, Y., et al. (2009) In Vivo MRI Identifies Cholinergic Circuitry Deficits in a Down Syndrome Model. Neurobiology of Aging, 30, 1453-1465. http://dx.doi.org/10.1016/j.neurobiolaging.2007.11.026
|
[48]
|
Filippi, C.G., et al. (2002) Developmental Delay in Children: Assessment with Proton MR Spectroscopy. American Journal of Neuroradiology, 23, 882-888.
|
[49]
|
Yao, F.S., Caserta, M.T. and Wyrwicz, A.M. (2000) In Vitro 1H and 31P NMR Spectroscopic Evidence of Multiple Aberrant Biochemical Pathways in Murine Trisomy 16 Brain Development. International Journal of Developmental Neuroscience, 18, 833-841. http://dx.doi.org/10.1016/S0736-5748(00)00043-5
|
[50]
|
Huang, W., et al. (2000) Brain Myo-Inositol Level Is Elevated in Ts65Dn Mouse and Reduced after Lithium Treatment. NeuroReport, 11, 445-448. http://dx.doi.org/10.1097/00001756-200002280-00004
|
[51]
|
Shetty, H.U., et al. (1996) Brain Accumulation of Myo-Inositol in the Trisomy 16 Mouse, an Animal Model of Down’s Syndrome. Biochemical Journal, 313, 31-33.
|
[52]
|
Morris, R.G., et al. (1982) Place Navigation Impaired in Rats with Hippocampal Lesions. Nature, 297, 681-683. http://dx.doi.org/10.1038/297681a0
|
[53]
|
Fernandez, F. and Garner, C.C. (2008) Episodic-Like Memory in Ts65Dn, a Mouse Model of Down Syndrome. Behavioural Brain Research, 188, 233-237. http://dx.doi.org/10.1016/j.bbr.2007.09.015
|
[54]
|
Demas, G.E., et al. (1996) Spatial Memory Deficits in Segmental Trisomic Ts65Dn Mice. Behavioural Brain Research, 82, 85-92. http://dx.doi.org/10.1016/S0166-4328(97)81111-4
|
[55]
|
Kleschevnikov, A.M., et al. (2004) Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome. The Journal of Neuroscience, 24, 8153-8160. http://dx.doi.org/10.1523/JNEUROSCI.1766-04.2004
|
[56]
|
Galdzicki, Z. and Siarey, R.J. (2003) Understanding Mental Retardation in Down’s Syndrome Using Trisomy 16 Mouse Models. Genes, Brain and Behavior, 2, 167-178. http://dx.doi.org/10.1034/j.1601-183X.2003.00024.x
|
[57]
|
Kurt, M.A., et al. (2004) Deficits of Neuronal Density in CA1 and Synaptic Density in the Dentate Gyrus, CA3 and CA1, in a Mouse Model of Down Syndrome. Brain Research, 1022, 101-109. http://dx.doi.org/10.1016/j.brainres.2004.06.075
|
[58]
|
Gotti, S., Caricati, E. and Panzica, G. (2011) Alterations of Brain Circuits in Down Syndrome Murine Models. Journal of Chemical Neuroanatomy, 42, 317-326. http://dx.doi.org/10.1016/j.jchemneu.2011.09.002
|
[59]
|
Lorenzi, H.A. and Reeves, R.H. (2006) Hippocampal Hypocellularity in the Ts65Dn Mouse Originates Early in Development. Brain Research, 1104, 153-159. http://dx.doi.org/10.1016/j.brainres.2006.05.022
|
[60]
|
Popov, V.I., et al. (2011) Three-Dimensional Synaptic Ultrastructure in the Dentate Gyrus and Hippocampal Area CA3 in the Ts65Dn Mouse Model of Down Syndrome. Journal of Comparative Neurology, 519, 1338-1354. http://dx.doi.org/10.1002/cne.22573
|
[61]
|
Dickson, P.E., et al. (2010) Behavioral Flexibility in a Mouse Model of Developmental Cerebellar Purkinje Cell Loss. Neurobiology of Learning and Memory, 94, 220-228. http://dx.doi.org/10.1016/j.nlm.2010.05.010
|
[62]
|
Contestabile, A., et al. (2009) Cell Cycle Elongation Impairs Proliferation of Cerebellar Granule Cell Precursors in the Ts65Dn Mouse, an Animal Model for Down Syndrome. Brain Pathology, 19, 224-237. http://dx.doi.org/10.1111/j.1750-3639.2008.00168.x
|
[63]
|
Olson, L.E., et al. (2004) Down Syndrome Mouse Models Ts65Dn, Ts1Cje, and Ms1Cje/Ts65Dn Exhibit Variable Severity of Cerebellar Phenotypes. Developmental Dynamics, 230, 581-589. http://dx.doi.org/10.1002/dvdy.20079
|
[64]
|
Marjanska, M., et al. (2005) Monitoring Disease Progression in Transgenic Mouse Models of Alzheimer’s Disease with Proton Magnetic Resonance Spectroscopy. Proceedings of the National Academy of Sciences of the United States of America, 102, 11906-11910. http://dx.doi.org/10.1073/pnas.0505513102
|
[65]
|
Miyasaka, N., Takahashi, K. and Hetherington, H.P. (2006) 1H NMR Spectroscopic Imaging of the Mouse Brain at 9.4T. Journal of Magnetic Resonance Imaging, 24, 908-913. http://dx.doi.org/10.1002/jmri.20709
|
[66]
|
Hsu, Y.Y., et al. (2001) Lateralization and Prognostic Value of Proton Magnetic Resonance Spectroscopy in Patients with Intractable Temporal Lobe Epilepsy. Chang Gung Medical Journal, 24, 768-778.
|
[67]
|
Jessen, F., et al. (2000) Proton MR Spectroscopy Detects a Relative Decrease of N-Acetylaspartate in the Medial Temporal Lobe of Patients with AD. Neurology, 55, 684-688. http://dx.doi.org/10.1212/WNL.55.5.684
|
[68]
|
Bambrick, L.L., Yarowsky, P.J. and Krueger, B.K. (2003) Altered Astrocyte Calcium Homeostasis and Proliferation in the Ts65Dn Mouse, a Model of Down Syndrome. Journal of Neuroscience Research, 73, 89-94. http://dx.doi.org/10.1002/jnr.10630
|
[69]
|
Brand, A., Richter-Landsberg, C. and Leibfritz, D. (1993) Multinuclear NMR Studies on the Energy Metabolism of Glial and Neuronal Cells. Developmental Neuroscience, 15, 289-298. http://dx.doi.org/10.1159/000111347
|
[70]
|
Ceuterick, C., et al. (1998) Astroglial Tangles in the Hippocampus of Two Patients with Down Syndrome and Alzheimer Neuropathology. Ultrastructural Pathology, 22, 161-163. http://dx.doi.org/10.3109/01913129809032272
|
[71]
|
Jorgensen, O.S., Brooksbank, B.W. and Balazs, R. (1990) Neuronal Plasticity and Astrocytic Reaction in Down Syndrome and Alzheimer Disease. Journal of the Neurological Sciences, 98, 63-79. http://dx.doi.org/10.1016/0022-510X(90)90182-M
|
[72]
|
Murphy Jr., G.M., et al. (1992) Astrocytic Gliosis in the Amygdala in Down’s Syndrome and Alzheimer’s Disease. Progress in Brain Research, 94, 475-483. http://dx.doi.org/10.1016/S0079-6123(08)61774-4
|
[73]
|
Belichenko, P.V., et al. (2007) Synaptic and Cognitive Abnormalities in Mouse Models of Down Syndrome: Exploring Genotype-Phenotype Relationships. Journal of Comparative Neurology, 504, 329-345. http://dx.doi.org/10.1002/cne.21433
|
[74]
|
Belichenko, N.P., et al. (2009) The “Down Syndrome Critical Region” Is Sufficient in the Mouse Model to Confer Behavioral, Neurophysiological, and Synaptic Phenotypes Characteristic of Down Syndrome. The Journal of Neuroscience, 29, 5938-5948. http://dx.doi.org/10.1523/JNEUROSCI.1547-09.2009
|
[75]
|
Kleschevnikov, A.M., et al. (2012) Increased Efficiency of the GABAA and GABAB Receptor-Mediated Neurotransmission in the Ts65Dn Mouse Model of Down Syndrome. Neurobiology of Disease, 45, 683-691. http://dx.doi.org/10.1016/j.nbd.2011.10.009
|
[76]
|
Dierssen, M., et al. (1997) Alterations of Central Noradrenergic Transmission in Ts65Dn Mouse, a Model for Down Syndrome. Brain Research, 749, 238-244. http://dx.doi.org/10.1016/S0006-8993(96)01173-0
|
[77]
|
Dierssen, M., et al. (1996) Impaired Cyclic AMP Production in the Hippocampus of a Down Syndrome Murine Model. Developmental Brain Research, 95, 122-124. http://dx.doi.org/10.1016/0165-3806(96)00071-5
|
[78]
|
Duchon, A., et al. (2011) The Telomeric Part of the Human Chromosome 21 from Cstb to Prmt2 Is Not Necessary for the Locomotor and Short-Term Memory Deficits Observed in the Tc1 Mouse Model of Down Syndrome. Behavioural Brain Research, 217, 271-281. http://dx.doi.org/10.1016/j.bbr.2010.10.023
|
[79]
|
Gruetter, R. (1993) Automatic, Localized in Vivo Adjustment of All Firstand Second-Order Shim Coils. Magnetic Resonance in Medicine, 29, 804-811. http://dx.doi.org/10.1002/mrm.1910290613
|
[80]
|
Tkac, I., et al. (1999) In Vivo 1H NMR Spectroscopy of Rat Brain at 1 ms Echo Time. Magnetic Resonance in Medicine, 41, 649-656. http://dx.doi.org/10.1002/(SICI)1522-2594(199904)41:4<649::AID-MRM2>3.0.CO;2-G
|
[81]
|
Vanhamme, L., van den Boogaart, A. and Van Huffel, S. (1997) Improved Method for Accurate and Efficient Quantification of MRS Data with Use of Prior Knowledge. Journal of Magnetic Resonance, 129, 35-43. http://dx.doi.org/10.1006/jmre.1997.1244
|
[82]
|
van Eijsden, P., et al. (2010) In Vivo Neurochemical Profiling of Rat Brain by 1H-[13C] NMR Spectroscopy: Cerebral Energetics and Glutamatergic/GABAergic Neurotransmission. Journal of Neurochemistry, 112, 24-33. http://dx.doi.org/10.1111/j.1471-4159.2009.06428.x
|
[83]
|
Xin, L., et al. (2010) 1H-[13C] NMR Spectroscopy of the Rat Brain during Infusion of [2-13C] Acetate at 14.1 T. Magnetic Resonance in Medicine, 64, 334-340.
|