PHF and PHF-like fibrils –cause or consequence?
暂无分享,去创建一个
[1] P. Silver,et al. Polyglutamine Expansions Proteolysis, Chaperones, and the Dangers of Promiscuity , 2000, Neuron.
[2] Y. Ihara,et al. Neurofibrillary tangle-associated collapsin response mediator protein-2 (CRMP-2) is highly phosphorylated on Thr-509, Ser-518, and Ser-522. , 2000, Biochemistry.
[3] 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.
[4] 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.
[5] Y. Ihara,et al. Stable expression in Chinese hamster ovary cells of mutated tau genes causing frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). , 1999, The American journal of pathology.
[6] P. Coleman,et al. Neurons may live for decades with neurofibrillary tangles. , 1999, Journal of neuropathology and experimental neurology.
[7] John X. Morris,et al. Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17. , 1998, Science.
[8] M. Goedert,et al. Tau proteins with FTDP‐17 mutations have a reduced ability to promote microtubule assembly , 1998, FEBS letters.
[9] B. Sommer,et al. Neuron loss in APP transgenic mice , 1998, Nature.
[10] P. Mcgeer,et al. Pyramidal neuron loss is matched by ghost tangle increase in Guam parkinsonism-dementia hippocampus , 1998, Acta Neuropathologica.
[11] Y. Ihara,et al. Collapsin Response Mediator Protein-2 Is Associated with Neurofibrillary Tangles in Alzheimer’s Disease* , 1998, The Journal of Biological Chemistry.
[12] B. Ghetti,et al. Frontotemporal Dementia and Parkinsonism Linked to Chromosome 17: A New Group of Tauopathies , 1998, Brain pathology.
[13] B. Hyman,et al. Aβ Deposition Is Associated with Neuropil Changes, but not with Overt Neuronal Loss in the Human Amyloid Precursor Protein V717F (PDAPP) Transgenic Mouse , 1997, The Journal of Neuroscience.
[14] 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.
[15] M. Omary,et al. Stress, Apoptosis, and Mitosis Induce Phosphorylation of Human Keratin 8 at Ser-73 in Tissues and Cultured Cells* , 1997, The Journal of Biological Chemistry.
[16] Richard Hollister,et al. Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease , 1997, Annals of neurology.
[17] S. Younkin,et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.
[18] 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.
[19] Nigel J. Cairns,et al. Neurons, intracellular and extracellular neurofibrillary tangles in subdivisions of the hippocampal cortex in normal ageing and Alzheimer's disease , 1995, Neuroscience Letters.
[20] R. Wolfert,et al. Reduction of β‐amyloid peptide42 in the cerebrospinal fluid of patients with Alzheimer's disease , 1995 .
[21] L. Mucke,et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.
[22] J. Trojanowski,et al. Biopsy-derived adult human brain tau is phosphorylated at many of the same sites as Alzheimer's disease paired helical filament tau , 1994, Neuron.
[23] Y. Ihara. Massive somatodendritic sprouting of cortical neurons in Alzheimer's disease , 1988, Brain Research.
[24] D. Neary,et al. THE PROGRESSION OF THE PATHOLOGICAL CHANGES OF ALZHEIMER'S DISEASE IN FRONTAL AND TEMPORAL NEOCORTEX EXAMINED BOTH AT BIOPSY AND AT AUTOPSY , 1988, Neuropathology and applied neurobiology.
[25] K. Zatloukal,et al. Hepatocyte cytokeratins are hyperphosphorylated at multiple sites in human alcoholic hepatitis and in a mallory body mouse model. , 2000, The American journal of pathology.
[26] G. Reynolds. Banbury Report 15, Biological Aspects of Alzheimer's Disease: edited by R. Katzman, Cold Spring Harbor Laboratory, 1983. US $55.00 ($66.00 outside US) (xiv + 495 pages) ISBN 0 87969 213 8 , 1984 .