The Value of Transgenic Models for the Study of Neurodegenerative Diseases
暂无分享,去创建一个
D. Borchelt | D. Price | P. Wong | D. Cleveland | S. Sisodia | Michael K. Lee | DONALD L. PRICE | A. Markowska | Gopal Thinakaren | PHILIP C. WONG | ALICJA L. MARKOWSKA | MICHAEL K. LEE | GOPAL THINAKAREN | DONALD W. CLEVELAND | SANGRAM S. SISODIA | DAVID R. BORCHELT
[1] S. W. Davies,et al. Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic Mice , 1996, Cell.
[2] M. Gurney,et al. Enhanced oxygen radical production in a transgenic mouse model of familial amyotrophic lateral sclerosis , 1998, Annals of neurology.
[3] J. Hardy,et al. Alzheimer's disease: In search of γ-secretase , 1999, Nature.
[4] Q. Zhu,et al. Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[5] V. Culotta,et al. Chaperone-facilitated copper binding is a property common to several classes of familial amyotrophic lateral sclerosis-linked superoxide dismutase mutants. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[6] D. Selkoe,et al. Translating cell biology into therapeutic advances in Alzheimer's disease , 1999, Nature.
[7] R. Motter,et al. Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse , 1999, Nature.
[8] D. Borchelt,et al. ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions , 1997, Neuron.
[9] Mark Turmaine,et al. Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation , 1997, Cell.
[10] Robert H. Brown,et al. Increased 3‐nitrotyrosine in both sporadic and familial amyotrophic lateral sclerosis , 1997, Annals of neurology.
[11] Robert H. Brown,et al. Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis , 1997, Journal of neurochemistry.
[12] Robert H. Brown,et al. Amyotrophic lateral sclerosis. Insights from genetics. , 1997, Archives of neurology.
[13] M. Gurney,et al. The Copper Chelator d‐Penicillamine Delays Onset of Disease and Extends Survival in a Transgenic Mouse Model of Familial Amyotrophic Lateral Sclerosis , 1997, The European journal of neuroscience.
[14] S. Prusiner,et al. Doxycycline control of prion protein transgene expression modulates prion disease in mice. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[15] D. Selkoe,et al. Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity , 1999, Nature.
[16] P. Wong,et al. Pathogenesis of two axonopathies does not require axonal neurofilaments , 1998, Nature.
[17] S. Tonegawa,et al. Skeletal and CNS Defects in Presenilin-1-Deficient Mice , 1997, Cell.
[18] D. Price,et al. Loss of the Presynaptic Vesicle Protein Synaptophysin in Hippocampus Correlates with Cognitive Decline in Alzheimer Disease , 1997, Journal of neuropathology and experimental neurology.
[19] J. Hardy,et al. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes , 1998, Nature Medicine.
[20] P N Leigh,et al. Excitotoxicity in ALS , 1996, Neurology.
[21] M. Jackson,et al. Gene expression profiles of laser-captured adjacent neuronal subtypes , 1999, Nature Medicine.
[22] C. van Broeckhoven,et al. Molecular genetics of Alzheimer's disease. , 1998, Annals of medicine.
[23] D. Cleveland. From Charcot to SOD1 Mechanisms of Selective Motor Neuron Death in ALS , 1999, Neuron.
[24] J. Hardy,et al. Genetic classification of primary neurodegenerative disease. , 1998, Science.
[25] M. Alexander,et al. Principles of Neural Science , 1981 .
[26] D. Borchelt,et al. Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin. , 1999, Human molecular genetics.
[27] D. Borchelt,et al. Motor neuron disease caused by mutations in superoxide dismutase 1. , 1995, Current opinion in neurology.
[28] Bruce A. Yankner,et al. Aging renders the brain vulnerable to amyloid β-protein neurotoxicity , 1998, Nature Medicine.
[29] S. Carpenter. Proximal axonal enlargement in motor neuron disease , 1968, Neurology.
[30] L. Liotta,et al. Immuno-LCM: laser capture microdissection of immunostained frozen sections for mRNA analysis. , 1999, The American journal of pathology.
[31] Andreas Weidemann,et al. Identification, biogenesis, and localization of precursors of Alzheimer's disease A4 amyloid protein , 1989, Cell.
[32] J. Julien,et al. Progressive neuronopathy in transgenic mice expressing the human neurofilament heavy gene: A mouse model of amyotrophic lateral sclerosis , 1993, Cell.
[33] M. Albert,et al. Cognitive and neurobiologic markers of early Alzheimer disease. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[34] L. Liotta,et al. Laser-capture microdissection: opening the microscopic frontier to molecular analysis. , 1998, Trends in genetics : TIG.
[35] J. Morris,et al. Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease , 1999, Annals of neurology.
[36] A. Peterson,et al. Neurofilament-deficient axons and perikaryal aggregates in viable transgenic mice expressing a neurofilament-β-galactosidase fusion protein , 1994, Neuron.
[37] M. Gurney,et al. Development of central nervous system pathology in a murine transgenic model of human amyotrophic lateral sclerosis. , 1994, The American journal of pathology.
[38] J. Morrison,et al. Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[39] D. Price,et al. The Copper Chaperone CCS Is Abundant in Neurons and Astrocytes in Human and Rodent Brain , 1999, Journal of neurochemistry.
[40] D. Borchelt,et al. Mutations associated with amyotrophic lateral sclerosis convert superoxide dismutase from an antiapoptotic gene to a proapoptotic gene: studies in yeast and neural cells. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[41] S. Lippard. Free Copper Ions in the Cell? , 1999, Science.
[42] R. Casareno,et al. The Copper Chaperone for Superoxide Dismutase* , 1997, The Journal of Biological Chemistry.
[43] D L Price,et al. Copper chaperone for superoxide dismutase is essential to activate mammalian Cu/Zn superoxide dismutase. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[44] M. Gurney,et al. A low expressor line of transgenic mice carrying a mutant human Cu,Zn superoxide dismutase (SOD1) gene develops pathological changes that most closely resemble those in human amyotrophic lateral sclerosis , 1997, Acta Neuropathologica.
[45] Í. Lopes-Cendes,et al. The Neuropathology of CAG Repeat Diseases: Review and Update of Genetic and Molecular Features , 1997, Brain pathology.
[46] Rainer M. Bohle,et al. Real-time quantitative RT–PCR after laser-assisted cell picking , 1998, Nature Medicine.
[47] Junying Yuan,et al. Inhibition of ICE slows ALS in mice , 1997, Nature.
[48] M. Pericak-Vance,et al. Amyotrophic lateral sclerosis and structural defects in Cu,Zn superoxide dismutase. , 1993, Science.
[49] H. Zoghbi,et al. Expanding Our Understanding of Polyglutamine Diseases through Mouse Models , 1999, Neuron.
[50] D. Price,et al. Expression of Presenilin 1 and 2 (PS1 and PS2) in Human and Murine Tissues , 1996, The Journal of Neuroscience.
[51] D L Price,et al. Genetic neurodegenerative diseases: the human illness and transgenic models. , 1998, Science.
[52] Bin Zhang,et al. Age-Dependent Emergence and Progression of a Tauopathy in Transgenic Mice Overexpressing the Shortest Human Tau Isoform , 1999, Neuron.
[53] D. Borchelt,et al. Endoproteolysis of Presenilin 1 and Accumulation of Processed Derivatives In Vivo , 1996, Neuron.
[54] D. Westaway,et al. Alzheimer's disease: Antibody clears senile plaques , 1999, Nature.
[55] Ole A. Andreassen,et al. Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis , 1999, Nature Medicine.
[56] M. H. Angelis,et al. Maintenance of somite borders in mice requires the Delta homologue Dll1 , 1997, Nature.
[57] M. Gurney,et al. Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. , 1994, Science.
[58] P. Lansbury. Evolution of amyloid: what normal protein folding may tell us about fibrillogenesis and disease. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[59] E. Stadtman. Protein oxidation and aging , 2006, Science.
[60] M. Mesulam. Neuroplasticity Failure in Alzheimer's Disease Bridging the Gap between Plaques and Tangles , 1999, Neuron.
[61] O. Puciłowski,et al. [Neurotransmitters and neuropeptides]. , 1983, Polski tygodnik lekarski.
[62] J. Morrison,et al. Time course of neuropathology in the spinal cord of G86R superoxide dismutase transgenic mice , 1998, The Journal of comparative neurology.
[63] J. Elliott. Experimental Models of Amyotrophic Lateral Sclerosis , 1999, Neurobiology of Disease.
[64] B. Sommer,et al. Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[65] S. Younkin,et al. An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants. , 1994, Science.
[66] D. Borchelt,et al. Axonal Transport of Mutant Superoxide Dismutase 1 and Focal Axonal Abnormalities in the Proximal Axons of Transgenic Mice , 1998, Neurobiology of Disease.
[67] S. Sisodia. Beta-amyloid precursor protein cleavage by a membrane-bound protease. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[68] Hugo Vanderstichele,et al. Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.
[69] E. Kandel,et al. Inducible and Reversible Gene Expression with the rtTA System for the Study of Memory , 1998, Neuron.
[70] J. Trojanowski,et al. Neurofilaments and Orthograde Transport Are Reduced in Ventral Root Axons of Transgenic Mice that Express Human SOD1 with a G93A Mutation , 1997, The Journal of cell biology.
[71] B. Hyman,et al. APPSW Transgenic Mice Develop Age‐related Aβ Deposits and Neuropil Abnormalities, but no Neuronal Loss in CA1 , 1997, Journal of neuropathology and experimental neurology.
[72] T. O’Halloran,et al. Multiple Protein Domains Contribute to the Action of the Copper Chaperone for Superoxide Dismutase* , 1999, The Journal of Biological Chemistry.
[73] D. Price,et al. The genetic and molecular mechanisms of motor neuron disease , 1998, Current Opinion in Neurobiology.
[74] D. Borchelt,et al. Corrigendum: Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin (Human Molecular Genetics (1999) 8 (397-407)) , 1999 .
[75] D. Bredesen,et al. Altered Reactivity of Superoxide Dismutase in Familial Amyotrophic Lateral Sclerosis , 1996, Science.
[76] E. Stadtman,et al. A gain-of-function of an amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutant: An enhancement of free radical formation due to a decrease in Km for hydrogen peroxide. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[77] I. Fridovich,et al. Superoxide dismutases. , 1975, Annual review of biochemistry.
[78] M. Mattson,et al. Protein modification by the lipid peroxidation product 4‐hydroxynonenal in the spinal cords of amyotrophic lateral sclerosis patients , 1998, Annals of neurology.
[79] S. Younkin,et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.
[80] J. Haines,et al. Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis , 1993, Nature.
[81] D. Price,et al. Evidence that beta-amyloid protein in Alzheimer's disease is not derived by normal processing. , 1990, Science.
[82] John Hardy,et al. Amyloid, the presenilins and Alzheimer's disease , 1997, Trends in Neurosciences.
[83] M. Dubois‐Dauphin,et al. Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis. , 1997, Science.
[84] D. Borchelt,et al. An Alzheimer's Disease-Linked PS1 Variant Rescues the Developmental Abnormalities of PS1-Deficient Embryos , 1998, Neuron.
[85] D. Borchelt,et al. Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins , 1997, Neuron.
[86] Harry T Orr,et al. SCA1 transgenic mice: A model for neurodegeneration caused by an expanded CAG trinucleotide repeat , 1995, Cell.
[87] J. Morrison,et al. Quantitative immunocytochemical analysis of the spinal cord in G86R superoxide dismutase transgenic mice: Neurochemical correlates of selective vulnerability , 1996, The Journal of comparative neurology.
[88] L. WilliamsonT,et al. 神経フィラメントの欠如は,家族性筋萎縮性側索硬化症関連スーパオキジドジスムターゼ1変異に対する運動ニューロンの選択的易損性を低下させ,疾患を遅らせる , 1998 .
[89] J. Gitlin,et al. The Role of Copper in Neurodegenerative Disease , 1999, Neurobiology of Disease.
[90] M. Gurney,et al. Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[91] J. Rossant,et al. Notch1 is required for the coordinate segmentation of somites. , 1995, Development.
[92] B. Sommer,et al. Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[93] D L Price,et al. A vector for expressing foreign genes in the brains and hearts of transgenic mice. , 1996, Genetic analysis : biomolecular engineering.
[94] D. Price,et al. Elevated free nitrotyrosine levels, but not protein-bound nitrotyrosine or hydroxyl radicals, throughout amyotrophic lateral sclerosis (ALS)-like disease implicate tyrosine nitration as an aberrant in vivo property of one familial ALS-linked superoxide dismutase 1 mutant. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[95] T. O’Halloran,et al. Undetectable intracellular free copper: the requirement of a copper chaperone for superoxide dismutase. , 1999, Science.
[96] G. Perry,et al. Identification and transport of full-length amyloid precursor proteins in rat peripheral nervous system , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[97] L. Bruijn,et al. Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. , 1998, Science.
[98] J. Kong,et al. Massive Mitochondrial Degeneration in Motor Neurons Triggers the Onset of Amyotrophic Lateral Sclerosis in Mice Expressing a Mutant SOD1 , 1998, The Journal of Neuroscience.
[99] Jean-Pierre Julien,et al. Neurofilament functions in health and disease , 1999, Current Opinion in Neurobiology.
[100] D. Borchelt,et al. Effects of PS1 Deficiency on Membrane Protein Trafficking in Neurons , 1998, Neuron.
[101] Richard A. Smith. Handbook of Amyotrophic Lateral Sclerosis , 1992 .
[102] D. Price,et al. Amyloid precursor protein in aged nonhuman primates. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[103] G. Dawson,et al. β-amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity , 1995, Cell.
[104] J. Gitlin,et al. Genetic and molecular basis for copper toxicity. , 1996, The American journal of clinical nutrition.
[105] D. Cleveland,et al. Slowing of axonal transport is a very early event in the toxicity of ALS–linked SOD1 mutants to motor neurons , 1999 .
[106] M. Gurney,et al. Benefit of vitamin E, riluzole, and gababapentin in a transgenic model of familial amyotrophic lateral sclerosis , 1996, Annals of neurology.
[107] M. Beal,et al. Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury , 1996, Nature Genetics.
[108] D. Borchelt,et al. An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria , 1995, Neuron.
[109] D. Price,et al. Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport. , 1990, Proceedings of the National Academy of Sciences of the United States of America.
[110] L. Mucke,et al. Comparison of Neurodegenerative Pathology in Transgenic Mice Overexpressing V717F β-Amyloid Precursor Protein and Alzheimer’s Disease , 1996, The Journal of Neuroscience.
[111] R. Barbour,et al. Purification and cloning of amyloid precursor protein β-secretase from human brain , 1999, Nature.
[112] A. Delacourte,et al. The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer’s disease , 1999, Neurology.
[113] J. Coyle,et al. Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain. , 1982, Science.
[114] D. Price,et al. Presenilin 1 is required for Notch 1 and Dll1 expression in the paraxial mesoderm , 1997, Nature.
[115] Alfredo G. Tomasselli,et al. Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity , 1999, Nature.
[116] A. Wernimont,et al. Crystal structure of the copper chaperone for superoxide dismutase , 1999, Nature Structural Biology.
[117] D. Borchelt,et al. Protein Topology of Presenilin 1 , 1996, Neuron.
[118] D. Borchelt,et al. Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[119] J. Buxbaum,et al. Alzheimer Amyloid Protein Precursor in the Rat Hippocampus: Transport and Processing through the Perforant Path , 1998, The Journal of Neuroscience.
[120] M. Frotscher,et al. Cerebral Amyloid Induces Aberrant Axonal Sprouting and Ectopic Terminal Formation in Amyloid Precursor Protein Transgenic Mice , 1999, The Journal of Neuroscience.
[121] S. W. Davies,et al. Intranuclear Neuronal Inclusions in Huntington's Disease and Dentatorubral and Pallidoluysian Atrophy: Correlation between the Density of Inclusions andIT15CAG Triplet Repeat Length , 1998, Neurobiology of Disease.
[122] J. Valentine,et al. Delivering Copper Inside Yeast and Human Cells , 1997, Science.
[123] John Q Trojanowski,et al. Neurodegenerative Tauopathies Human Disease and Transgenic Mouse Models , 1999, Neuron.
[124] D. Price,et al. Motor neurone disease and animal models , 1994, Neurobiology of Disease.
[125] Gurparkash Singh,et al. Mutant Human Presenilin 1 Protects presenilin 1 Null Mouse against Embryonic Lethality and Elevates Aβ1–42/43 Expression , 1998, Neuron.
[126] H. Zoghbi,et al. Polyglutamine diseases: protein cleavage and aggregation , 1999, Current Opinion in Neurobiology.
[127] R. Sherrington,et al. Presenilin Proteins Undergo Heterogeneous Endoproteolysis between Thr291and Ala299and Occur as Stable N- and C-Terminal Fragments in Normal and Alzheimer Brain Tissue , 1997, Neurobiology of Disease.
[128] T. Oltersdorf,et al. Cleavage of amyloid beta peptide during constitutive processing of its precursor. , 1990, Science.
[129] M. Pericak-Vance,et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease , 1991, Nature.
[130] A Hofman,et al. Estimation of the genetic contribution of presenilin-1 and -2 mutations in a population-based study of presenile Alzheimer disease. , 1998, Human molecular genetics.
[131] Q. Zhu,et al. Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[132] D. Selkoe,et al. Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production , 1992, Nature.
[133] M. Cudkowicz,et al. Limited corticospinal tract involvement in amyotrophic lateral sclerosis subjects with the A4V mutation in the copper/zinc superoxide dismutase gene , 1998, Annals of neurology.
[134] J. Roder,et al. Inducible gene expression in the nervous system of transgenic mice. , 1998, Annual review of neuroscience.
[135] B. Sommer,et al. Neuron loss in APP transgenic mice , 1998, Nature.
[136] J. Treanor,et al. Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.
[137] Robert H. Brown,et al. Superoxide Dismutase Activity, Oxidative Damage, and Mitochondrial Energy Metabolism in Familial and Sporadic Amyotrophic Lateral Sclerosis , 1993, Journal of neurochemistry.
[138] J. Morrison,et al. Life and death of neurons in the aging brain. , 1997, Science.
[139] B. Winblad,et al. A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloid , 1992, Nature Genetics.
[140] D. Pollen,et al. Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease , 1995, Nature.
[141] Shin Lin,et al. Metal ion chaperone function of the soluble Cu(I) receptor Atx1. , 1997, Science.
[142] M. Gurney,et al. Age-Dependent Penetrance of Disease in a Transgenic Mouse Model of Familial Amyotrophic Lateral Sclerosis , 1995, Molecular and Cellular Neuroscience.
[143] A Hirano,et al. Neuropathology of ALS , 1996, Neurology.
[144] D. Borchelt,et al. Superoxide Dismutase 1 Subunits with Mutations Linked to Familial Amyotrophic Lateral Sclerosis Do Not Affect Wild-type Subunit Function (*) , 1995, The Journal of Biological Chemistry.
[145] G. V. Van Hoesen,et al. The topographical and neuroanatomical distribution of neurofibrillary tangles and neuritic plaques in the cerebral cortex of patients with Alzheimer's disease. , 1991, Cerebral cortex.
[146] M. Beal,et al. Elevated “Hydroxyl Radical” Generation In Vivo in an Animal Model of Amyotrophic Lateral Sclerosis , 1998, Journal of neurochemistry.
[147] Christina A. Wilson,et al. Intracellular APP Processing and Aβ Production in Alzheimer Disease , 1999 .
[148] D L Price,et al. Alzheimer's disease: genetic studies and transgenic models. , 1998, Annual review of genetics.
[149] S. W. Davies,et al. Filamentous nerve cell inclusions in neurodegenerative diseases , 1998, Current Opinion in Neurobiology.
[150] D. Borchelt,et al. Caspase-1 is activated in neural cells and tissue with amyotrophic lateral sclerosis-associated mutations in copper-zinc superoxide dismutase. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[151] D. Price,et al. Mutant genes in familial Alzheimer's disease and transgenic models. , 1998, Annual review of neuroscience.
[152] L J Martin,et al. Neuronal death in amyotrophic lateral sclerosis is apoptosis: possible contribution of a programmed cell death mechanism. , 1999, Journal of neuropathology and experimental neurology.
[153] W. Rosenblum. The presence, origin, and significance of A beta peptide in the cell bodies of neurons. , 1999, Journal of neuropathology and experimental neurology.