PHF and PHF-like fibrils –cause or consequence?

[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 .