Cycles of Aberrant Synaptic Sprouting and Neurodegeneration in Alzheimer's and Dementia with Lewy Bodies
暂无分享,去创建一个
[1] K. Blennow,et al. Synaptic pathology in Alzheimer's disease: Relation to severity of dementia, but not to senile plaques, neurofibrillary tangles, or the ApoE4 allele , 2005, Journal of Neural Transmission.
[2] J. Häggendal. Noradrenaline and dopamine-beta-hydroxylase levels in rat salivary glands after preganglionic nerve stimulation: Evidence for re-use of amine storage granules in transmitter release , 2005, Journal of Neural Transmission.
[3] W. Honer,et al. Topographical distribution of synaptic-associated proteins in the neuritic plaques of Alzheimer's disease hippocampus , 2004, Acta Neuropathologica.
[4] E. Masliah,et al. Immunoelectron microscopic study of synaptic pathology in Alzheimer's disease , 2004, Acta Neuropathologica.
[5] H. Braak,et al. Neuropathological stageing of Alzheimer-related changes , 2004, Acta Neuropathologica.
[6] H. Braak,et al. A sequence of cytoskeleton changes related to the formation of neurofibrillary tangles and neuropil threads , 2004, Acta Neuropathologica.
[7] L. Thal,et al. Aβ1–42 promotes cholinergic sprouting in patients with AD and Lewy body variant of AD , 2003, Neurology.
[8] E. Masliah,et al. α‐Synuclein up‐regulates expression of caveolin‐1 and down‐regulates extracellular signal‐regulated kinase activity in B103 neuroblastoma cells: role in the pathogenesis of Parkinson's disease , 2003 .
[9] R. Malinow,et al. APP Processing and Synaptic Function , 2003, Neuron.
[10] P. Coleman,et al. Defects in expression of genes related to synaptic vesicle traffickingin frontal cortex of Alzheimer’s disease , 2003, Neurobiology of Disease.
[11] Smita Patel,et al. Golgi Fragmentation Occurs in the Cells with Prefibrillar α-Synuclein Aggregates and Precedes the Formation of Fibrillar Inclusion* , 2002, The Journal of Biological Chemistry.
[12] S. Totterdell,et al. Lysosomal malfunction accompanies alpha-synuclein aggregation in a progressive mouse model of Parkinson’s disease , 2002, Brain Research.
[13] W. Meier-Ruge,et al. Deafferentative Synaptopathology in Physiological Aging and Alzheimer's Disease , 2002, Annals of the New York Academy of Sciences.
[14] P. Greengard,et al. Intraneuronal Alzheimer abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology. , 2002, The American journal of pathology.
[15] Richard Paylor,et al. Synaptic Vesicle Depletion Correlates with Attenuated Synaptic Responses to Prolonged Repetitive Stimulation in Mice Lacking α-Synuclein , 2002, The Journal of Neuroscience.
[16] C. Rabiner,et al. Characterization of neuronal dystrophy induced by fibrillar amyloid β: implications for Alzheimer’s disease , 2002, Neuroscience.
[17] E. Masliah,et al. Fibroblast Growth Factor 1 Regulates Signaling via the Glycogen Synthase Kinase-3β Pathway , 2002, The Journal of Biological Chemistry.
[18] B. Hyman,et al. Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease. , 2002, Archives of neurology.
[19] Nancy A. Jenkins,et al. Human α-synuclein-harboring familial Parkinson's disease-linked Ala-53 → Thr mutation causes neurodegenerative disease with α-synuclein aggregation in transgenic mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[20] C. Masters,et al. Increased expression of the amyloid precursor β‐secretase in Alzheimer's disease , 2002 .
[21] T. Iwatsubo. [alpha-synuclein and Parkinson's disease]. , 2002, Seikagaku. The Journal of Japanese Biochemical Society.
[22] Bruce A. Yankner,et al. Dopamine-dependent neurotoxicity of α-synuclein: A mechanism for selective neurodegeneration in Parkinson disease , 2002, Nature Medicine.
[23] J. Trojanowski,et al. Neuronal α-Synucleinopathy with Severe Movement Disorder in Mice Expressing A53T Human α-Synuclein , 2002, Neuron.
[24] R. Doms,et al. β-Secretase Processing in the Trans-Golgi Network Preferentially Generates Truncated Amyloid Species That Accumulate in Alzheimer's Disease Brain* , 2002, The Journal of Biological Chemistry.
[25] Y. Sung,et al. α-Synuclein Interacts with Phospholipase D Isozymes and Inhibits Pervanadate-induced Phospholipase D Activation in Human Embryonic Kidney-293 Cells* , 2002, The Journal of Biological Chemistry.
[26] A. Björklund,et al. Parkinson-Like Neurodegeneration Induced by Targeted Overexpression of α-Synuclein in the Nigrostriatal System , 2002, The Journal of Neuroscience.
[27] E. Masliah,et al. α-Synuclein Protects against Oxidative Stress via Inactivation of the c-Jun N-terminal Kinase Stress-signaling Pathway in Neuronal Cells* , 2002, The Journal of Biological Chemistry.
[28] Patrik Brundin,et al. Pathogenesis of Parkinson's disease: dopamine, vesicles and alpha-synuclein. , 2002, Nature reviews. Neuroscience.
[29] Jürgen Götz,et al. Alzheimer's and Parkinson's disease--overlapping or synergistic pathologies? , 2002, Trends in molecular medicine.
[30] C. Masters,et al. Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease. , 2002, Annals of neurology.
[31] R. Doms,et al. Beta-secretase processing in the trans-Golgi network preferentially generates truncated amyloid species that accumulate in Alzheimer's disease brain. , 2002, The Journal of biological chemistry.
[32] J. Trojanowski,et al. Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein. , 2002, Neuron.
[33] M. Mattson,et al. Presenilins and APP in neuritic and synaptic plasticity , 2002, NeuroMolecular Medicine.
[34] I. Kanazawa,et al. α-Synuclein Affects the MAPK Pathway and Accelerates Cell Death* , 2001, The Journal of Biological Chemistry.
[35] Makoto Hashimoto,et al. β-Amyloid peptides enhance α-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[36] M. Wolfe,et al. A Portrait of Alzheimer Secretases--New Features and Familiar Faces , 2001, Science.
[37] V. Bigl,et al. Neuronal and glial β‐secretase (BACE) protein expression in transgenic Tg2576 mice with amyloid plaque pathology , 2001, Journal of neuroscience research.
[38] I. Kanazawa,et al. α‐Synuclein forms a complex with transcription factor Elk‐1 , 2001, Journal of neurochemistry.
[39] M. Linial,et al. Involvement of extracellular signal-regulated kinase (ERK) in pardaxin-induced dopamine release from PC12 cells. , 2001, The Journal of pharmacology and experimental therapeutics.
[40] E. Masliah,et al. Reduced Neuritic Outgrowth and Cell Adhesion in Neuronal Cells Transfected with Human α-Synuclein , 2001, Molecular and Cellular Neuroscience.
[41] E. Masliah,et al. Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease , 2001, Neurology.
[42] S. Scheff,et al. Alzheimer's disease-related synapse loss in the cingulate cortex. , 2001, Journal of Alzheimer's disease : JAD.
[43] L. Mucke,et al. beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease. , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[44] R. Mileusnic,et al. APP is required during an early phase of memory formation , 2000, The European journal of neuroscience.
[45] L. McConlogue,et al. Recent Advances in the Understanding of the Processing of APP to Beta Amyloid Peptide , 2000, Annals of the New York Academy of Sciences.
[46] Sarah J. Tabrizi,et al. Expression of mutant α-synuclein causes increased susceptibility to dopamine toxicity , 2000 .
[47] Mark P. Mattson,et al. Apoptosis in neurodegenerative disorders , 2000, Nature Reviews Molecular Cell Biology.
[48] D. Madison,et al. A Novel SNAP25–Caveolin Complex Correlates with the Onset of Persistent Synaptic Potentiation , 2000, The Journal of Neuroscience.
[49] E. Masliah,et al. α-Synuclein Promotes Mitochondrial Deficit and Oxidative Stress , 2000 .
[50] Kang Hu,et al. High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation , 2000, The Journal of Neuroscience.
[51] G. Glosser,et al. Alpha-synuclein cortical Lewy bodies correlate with dementia in Parkinson’s disease , 2000, Neurology.
[52] Y. Yang,et al. Enhanced vulnerability to oxidative stress by α-synuclein mutations and C-terminal truncation , 2000, Neuroscience.
[53] W. Bender,et al. A Drosophila model of Parkinson's disease , 2000, Nature.
[54] L. Mucke,et al. Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders. , 2000, Science.
[55] Heidi Phillips,et al. Mice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System , 2000, Neuron.
[56] E. Masliah,et al. alpha-synuclein promotes mitochondrial deficit and oxidative stress. , 2000, The American journal of pathology.
[57] Y. Yang,et al. Enhanced vulnerability to oxidative stress by alpha-synuclein mutations and C-terminal truncation. , 2000, Neuroscience.
[58] S. Tabrizi,et al. Expression of mutant alpha-synuclein causes increased susceptibility to dopamine toxicity. , 2000, Human molecular genetics.
[59] R. Barbour,et al. Purification and cloning of amyloid precursor protein β-secretase from human brain , 1999, Nature.
[60] J. Engelman,et al. Caveolins, Liquid-Ordered Domains, and Signal Transduction , 1999, Molecular and Cellular Biology.
[61] J. Treanor,et al. Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.
[62] E. Masliah,et al. Alpha‐synuclein in Lewy Body Disease and Alzheimer's Disease , 1999, Brain pathology.
[63] P. Lansbury,et al. Amyloid diseases: abnormal protein aggregation in neurodegeneration. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[64] R. Parton,et al. Membrane microdomains and caveolae. , 1999, Current opinion in cell biology.
[65] L. Petrucelli,et al. α-Synuclein Shares Physical and Functional Homology with 14-3-3 Proteins , 1999, The Journal of Neuroscience.
[66] D. Storm,et al. Making New Connections Role of ERK/MAP Kinase Signaling in Neuronal Plasticity , 1999, Neuron.
[67] 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.
[68] D. Salmon,et al. Neuropathological Correlates of Dementia in Alzheimer’s Disease , 1999 .
[69] P Choi,et al. alpha-Synuclein shares physical and functional homology with 14-3-3 proteins. , 1999, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[70] R. Jakes,et al. Effects of the mutations Ala30 to Pro and Ala53 to Thr on the physical and morphological properties of α‐synuclein protein implicated in Parkinson's disease , 1998, FEBS letters.
[71] Peter T. Lansbury,et al. Accelerated in vitro fibril formation by a mutant α-synuclein linked to early-onset Parkinson disease , 1998, Nature Medicine.
[72] Takeshi Iwatsubo,et al. Fatal attractions: abnormal protein aggregation and neuron death in Parkinson's disease and Lewy body dementia , 1998, Cell Death and Differentiation.
[73] Makoto Hashimoto,et al. Human recombinant NACP/α-synuclein is aggregated and fibrillated in vitro: Relevance for Lewy body disease , 1998, Brain Research.
[74] Hitoshi Takahashi,et al. α-Synuclein immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy , 1998, Neuroscience Letters.
[75] L. Mucke,et al. Amyloid Protein Precursor Stimulates Excitatory Amino Acid Transport , 1998, The Journal of Biological Chemistry.
[76] S. Love,et al. Frontal cortical synaptophysin in Lewy body diseases: relation to Alzheimer’s disease and dementia , 1998, Journal of neurology, neurosurgery, and psychiatry.
[77] M. Lisanti,et al. Caveolins, a Family of Scaffolding Proteins for Organizing “Preassembled Signaling Complexes” at the Plasma Membrane* , 1998, The Journal of Biological Chemistry.
[78] W. Honer,et al. Abnormal accumulation of NACP/alpha-synuclein in neurodegenerative disorders. , 1998, The American journal of pathology.
[79] Olaf Riess,et al. AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease , 1998, Nature Genetics.
[80] S. Younkin,et al. The APP and PS1/2 Mutations Linked to Early Onset Familial Alzheimer’s Disease Increase the Extracellular Concentration of Aβ1–42(43) , 1998 .
[81] S. Tsuji,et al. Alpha-synuclein immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy. , 1998, Neuroscience letters.
[82] E. Masliah,et al. Mechanisms of synaptic pathology in Alzheimer's disease. , 1998, Journal of neural transmission. Supplementum.
[83] R. Krüger,et al. Ala30Pro mutation in the gene encoding alpha-synuclein in Parkinson's disease. , 1998, Nature genetics.
[84] Hitoshi Takahashi,et al. NACP, a presynaptic protein, immunoreactivity in Lewy bodies in Parkinson's disease , 1997, Neuroscience Letters.
[85] S. Parsons,et al. Roles for Protein Kinase C and Mitogen‐Activated Protein Kinase in Nicotine‐Induced Secretion from Bovine Adrenal Chromaffin Cells , 1997, Journal of neurochemistry.
[86] M. L. Schmidt,et al. α-Synuclein in Lewy bodies , 1997, Nature.
[87] Robert L. Nussbaum,et al. Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease , 1997 .
[88] K. Blennow,et al. Synaptic Pathology in Alzheimer’s Disease , 1997 .
[89] S. Younkin. [The AAP and PS1/2 mutations linked to early onset familial Alzheimer's disease increase the extracellular concentration and A beta 1-42 (43)]. , 1997, Rinsho shinkeigaku = Clinical neurology.
[90] L. Hansen. The Lewy body variant of Alzheimer disease. , 1997, Journal of neural transmission. Supplementum.
[91] K. Kosaka,et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB) , 1996, Neurology.
[92] J. Hardy,et al. Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.
[93] 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.
[94] D. Selkoe,et al. The Role of APP Processing and Trafficking Pathways in the Formation of Amyloid β‐Protein a , 1996 .
[95] D. Galasko,et al. Neocortical Lewy Body Counts Correlate with Dementia in the Lewy Body Variant of Alzheimer's Disease , 1996, Journal of neuropathology and experimental neurology.
[96] D. Selkoe,et al. The role of APP processing and trafficking pathways in the formation of amyloid beta-protein. , 1996, Annals of the New York Academy of Sciences.
[97] W. Honer,et al. Correlations of synaptic and pathological markers with cognition of the elderly , 1995, Neurobiology of Aging.
[98] E. Masliah. Natural evolution of the neurodegenerative alterations in Alzheimer's disease , 1995, Neurobiology of Aging.
[99] S. M. Sumi,et al. The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part X. Neuropathology Confirmation of the Clinical Diagnosis of Alzheimer's Disease , 1995, Neurology.
[100] D. Selkoe,et al. beta-Amyloid, protein processing and Alzheimer's disease. , 1995, Arzneimittel-Forschung.
[101] Akihiko Iwai,et al. The precursor protein of non-Aβ component of Alzheimer's disease amyloid is a presynaptic protein of the central nervous system , 1995, Neuron.
[102] B. Anderson. DENDRITIC CORRELATES OF DEMENTIA SEVERITY IN ALZHEIMER'S DISEASE , 1995 .
[103] D.G. Jones,et al. An Analysis of Contemporary Morphological Concepts of Synaptic Remodelling in the CNS: Perforated Synapses Revisited , 1995, Reviews in the neurosciences.
[104] W. Honer,et al. Synapse alterations in the hippocampal-entorhinal formation in Alzheimer's disease with and without Lewy body disease , 1994, Brain Research.
[105] D. Price,et al. Synaptic pathology and glial responses to neuronal injury precede the formation of senile plaques and amyloid deposits in the aging cerebral cortex. , 1994, The American journal of pathology.
[106] L. R. Hill,et al. Hippocampal connectivity and Alzheimer's dementia , 1994, Neurology.
[107] L A Hansen,et al. Clinical-neuropathological correlations in Alzheimer's disease and related dementias. , 1994, Archives of neurology.
[108] E. Masliah,et al. Synaptic and neuritic alterations during the progression of Alzheimer's disease , 1994, Neuroscience Letters.
[109] J. Kimura,et al. Synaptophysin and chromogranin A immunoreactivities of Lewy bodies in Parkinson's disease brains , 1994, Brain Research.
[110] E. Masliah,et al. Structural basis of the cognitive alterations in Alzheimer disease. , 1994 .
[111] E. Masliah,et al. Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[112] D. Sparks,et al. Quantitative assessment of synaptic density in the entorhinal cortex in Alzheimer's disease , 1993, Annals of neurology.
[113] Michael Alford,et al. Differing patterns of aberrant neuronal sprouting in Alzheimer's disease with and without Lewy bodies , 1993, Brain Research.
[114] D. Selkoe,et al. Amyloid beta-protein as a substrate interacts with extracellular matrix to promote neurite outgrowth. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[115] K. Beyreuther,et al. Quantitative assessment of the synaptophysin immuno-reactivity of the cortical neuropil in various neurodegenerative disorders with dementia. , 1993, Dementia.
[116] D. Price,et al. Synapse loss in the temporal lobe in Alzheimer's disease , 1993, Annals of neurology.
[117] E. Masliah,et al. Amyloid precursor protein is localized in growing neurites of neonatal rat brain , 1992, Brain Research.
[118] J. Trojanowski,et al. Epitope analysis of senile plaque components in the hippocampus of patients with Parkinson's disease , 1992, Neurology.
[119] Brian J Cummings,et al. Aggregation of the amyloid precursor protein within degenerating neurons and dystrophic neurites in alzheimer's disease , 1992, Neuroscience.
[120] E. Masliah,et al. Localization of amyloid precursor protein in GAP43-immunoreactive aberrant sprouting neurites in Alzheimer's disease , 1992, Brain Research.
[121] Bradley T. Hyman,et al. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease , 1992, Neurology.
[122] K. Jellinger,et al. Synaptic pathology in alzheimer's disease: Immunological data for markers of synaptic and large dense-core vesicles , 1992, Neuroscience.
[123] M. Vandermeeren,et al. Neurite sprouting and cytoskeletal pathology in Alzheimer's disease: a comparative study with monoclonal antibodies to growth associated protein B-50 and paired helical filaments , 1992 .
[124] Walter Schubert,et al. Localization of Alzheimer βA4 amyloid precursor protein at central and peripheral synaptic sites , 1991, Brain Research.
[125] J. Hardy,et al. Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene , 1991, Nature.
[126] D. Salmon,et al. Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment , 1991, Annals of neurology.
[127] E. Masliah,et al. Abnormal brain spectrin immunoreactivity in sprouting neurons in Alzheimer disease , 1991, Neuroscience Letters.
[128] Fred H. Gage,et al. Reactive synaptogenesis assessed by synaptophysin immunoreactivity is associated with GAP-43 in the dentate gyrus of the adult rat , 1991, Experimental Neurology.
[129] Michael Alford,et al. Patterns of aberrant sprouting in alzheimer's disease , 1991, Neuron.
[130] M. Pericak-Vance,et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease , 1991, Nature.
[131] Carl W. Cotman,et al. The Role of Misdirected Plasticity in Plaque Biogenesis and Alzheimer's Disease Pathology , 1991 .
[132] E. Masliah,et al. Cortical and subcortical patterns of synaptophysinlike immunoreactivity in Alzheimer's disease. , 1991, The American journal of pathology.
[133] D. Price,et al. Development of senile plaques. Relationships of neuronal abnormalities and amyloid deposits. , 1990, The American journal of pathology.
[134] D. Kirschner,et al. Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. , 1990, Science.
[135] D. Price,et al. RELATIONSHIPS OF ABNORMAL NEURONAL PROCESSES AND AMYLOID IN PLAQUES IN AGED MONKEYS: 146 , 1990 .
[136] S. DeKosky,et al. Synapse loss in frontal cortex biopsies in Alzheimer's disease: Correlation with cognitive severity , 1990, Annals of neurology.
[137] K. Jellinger,et al. A high ratio of chromogranin A to synaptin/synaptophysin is a common feature of brains in Alzheimer and Pick disease , 1990, FEBS letters.
[138] R. Katzman.,et al. Alzheimer's disease is a degenerative disorder , 1989, Neurobiology of Aging.
[139] E. Masliah,et al. Immunohistochemical quantification of the synapse-related protein synaptophysin in Alzheimer disease , 1989, Neuroscience Letters.
[140] David A. Drachman,et al. Synaptic loss in Alzheimer's disease and other dementias , 1989, Neurology.
[141] D. Dickson,et al. Alzheimer's disease. A double-labeling immunohistochemical study of senile plaques. , 1988, The American journal of pathology.
[142] C. Cotman,et al. Synaptic plasticity and functional stabilization in the hippocampal formation: possible role in Alzheimer's disease. , 1988, Advances in neurology.
[143] D. Mann,et al. A quantitative morphometric analysis of the neuronal and synaptic content of the frontal and temporal cortex in patients with Alzheimer's disease , 1987, Journal of the Neurological Sciences.
[144] R. Mayeux,et al. Diffuse Lewy body disease. Neuropathological and biochemical studies of six patients. , 1987, Acta neuropathologica.
[145] C. Cotman,et al. Senile plaques as aberrant sprout-stimulating structures , 1986, Experimental Neurology.
[146] Z. Khachaturian. Diagnosis of Alzheimer's disease. , 1985, Archives of neurology.
[147] K Kosaka,et al. Diffuse type of Lewy body disease: progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree--a new disease? , 1984, Clinical neuropathology.
[148] J. Eccles. The Cerebral Neocortex , 1984 .
[149] O. Steward,et al. Synaptic replacement in the dentate gyrus after unilateral entorhinal lesion: electron microscopic analysis of the extent of replacement of synapses by the remaining entorhinal cortex , 1977, Journal of neurocytology.
[150] Gary Lynch,et al. An electron microscopic study of lesion-induced synaptogenesis in the dentate gyrus of the adult rat. II. Reappearance of morphologically normal synaptic contacts , 1976, Brain Research.
[151] G. Lynch,et al. Spine Loss and Regrowth in Hippocampus following Deafferentation , 1974, Nature.
[152] G. Lynch,et al. A quantitative electron microscopic study of synaptogenesis in the dentate gyrus of the rat. , 1973, Brain research.
[153] G. Lynch,et al. Synaptic rearrangement in the dentate gyrus: histochemical evidence of adjustments after lesions in immature and adult rats. , 1973, Proceedings of the National Academy of Sciences of the United States of America.
[154] I. Evangelista,et al. THE CONTRIBUTION OF ALTERED SYNAPSES IN THE SENILE PLAQUE: AN ELECTRON MICROSCOPIC STUDY IN ALZHEIMER'S DEMENTIA , 1967, Journal of neuropathology and experimental neurology.
[155] R. Terry,et al. ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA. , 1964, The American journal of pathology.