Aβ localization in abnormal endosomes: association with earliest Aβ elevations in AD and Down syndrome

[1]  H. Braak,et al.  Neuropathological stageing of Alzheimer-related changes , 2004, Acta Neuropathologica.

[2]  S. Schmidt,et al.  Rab5-stimulated Up-regulation of the Endocytic Pathway Increases Intracellular β-Cleaved Amyloid Precursor Protein Carboxyl-terminal Fragment Levels and Aβ Production* , 2003, Journal of Biological Chemistry.

[3]  C. Epstein,et al.  App Gene Dosage Modulates Endosomal Abnormalities of Alzheimer's Disease in a Segmental Trisomy 16 Mouse Model of Down Syndrome , 2003, The Journal of Neuroscience.

[4]  Carl W. Cotman,et al.  Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.

[5]  J. Hardy,et al.  The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .

[6]  J. Rohrer,et al.  Alzheimer's Disease-related Overexpression of the Cation-dependent Mannose 6-Phosphate Receptor Increases Aβ Secretion , 2002, The Journal of Biological Chemistry.

[7]  S. Green,et al.  Endosomal Sorting of Amyloid Precursor Protein‐P‐Selectin Chimeras Influences Secretase Processing , 2001, Traffic.

[8]  J. Troncoso,et al.  Intraneuronal abeta-amyloid precedes development of amyloid plaques in Down syndrome. , 2001, Archives of pathology & laboratory medicine.

[9]  R. Doms,et al.  Maturation and Endosomal Targeting of β-Site Amyloid Precursor Protein-cleaving Enzyme , 2000, The Journal of Biological Chemistry.

[10]  J. Rohrer,et al.  A Di-aromatic Motif in the Cytosolic Tail of the Mannose Receptor Mediates Endosomal Sorting* , 2000, The Journal of Biological Chemistry.

[11]  A. Levey,et al.  Endogenous Presenilin-1 Targets to Endocytic Rather Than Biosynthetic Compartments , 2000, Molecular and Cellular Neuroscience.

[12]  B T Hyman,et al.  Endocytic pathway abnormalities precede amyloid beta deposition in sporadic Alzheimer's disease and Down syndrome: differential effects of APOE genotype and presenilin mutations. , 2000, The American journal of pathology.

[13]  K. Davis,et al.  Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline. , 2000, JAMA.

[14]  P. Greengard,et al.  Intraneuronal Aβ42 Accumulation in Human Brain , 2000 .

[15]  H. Wiśniewski,et al.  Plasma and cerebrospinal fluid Levels of amyloid β proteins 1-40 and 1-42 in Alzheimer disease , 2000 .

[16]  C. Masters,et al.  Soluble pool of Aβ amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease , 1999, Annals of neurology.

[17]  Virginia M. Y. Lee,et al.  Expression of β-Amyloid Precursor Protein-CD3γ Chimeras to Demonstrate the Selective Generation of Amyloid β1–40and Amyloid β1–42 Peptides within Secretory and Endocytic Compartments* , 1999, The Journal of Biological Chemistry.

[18]  J. Treanor,et al.  Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.

[19]  Dominic M. Walsh,et al.  Protofibrillar Intermediates of Amyloid β-Protein Induce Acute Electrophysiological Changes and Progressive Neurotoxicity in Cortical Neurons , 1999, The Journal of Neuroscience.

[20]  L. Lue,et al.  Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease , 1999 .

[21]  J. Trojanowski,et al.  The Levels of Soluble versus Insoluble Brain Aβ Distinguish Alzheimer's Disease from Normal and Pathologic Aging , 1999, Experimental Neurology.

[22]  D. Selkoe,et al.  Mutagenesis Identifies New Signals for β-Amyloid Precursor Protein Endocytosis, Turnover, and the Generation of Secreted Fragments, Including Aβ42* , 1999, The Journal of Biological Chemistry.

[23]  P. Greengard,et al.  Endoplasmic reticulum and trans-Golgi network generate distinct populations of Alzheimer beta-amyloid peptides. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[24]  Yutaka Kirino,et al.  Cleavage of Alzheimer’s Amyloid Precursor Protein (APP) by Secretases Occurs after O-Glycosylation of APP in the Protein Secretory Pathway , 1998, The Journal of Biological Chemistry.

[25]  B. Greenberg,et al.  Turnover of Amyloid β-Protein in Mouse Brain and Acute Reduction of Its Level by Phorbol Ester , 1998, The Journal of Neuroscience.

[26]  K. Beyreuther,et al.  Late Compartments of Amyloid Precursor Protein Transport in SY5Y Cells Are Involved in β-Amyloid Secretion , 1997, The Journal of Neuroscience.

[27]  R. Doms,et al.  Alzheimer's Aβ(1–42) is generated in the endoplasmic reticulum/intermediate compartment of NT2N cells , 1997, Nature Medicine.

[28]  C. Masters,et al.  Distinct sites of intracellular production for Alzheimer's disease Aβ40/42 amyloid peptides , 1997, Nature Medicine.

[29]  R. Nixon,et al.  Increased Neuronal Endocytosis and Protease Delivery to Early Endosomes in Sporadic Alzheimer’s Disease: Neuropathologic Evidence for a Mechanism of Increased β-Amyloidogenesis , 1997, The Journal of Neuroscience.

[30]  R. Doms,et al.  Novel β-Secretase Cleavage of β-Amyloid Precursor Protein in the Endoplasmic Reticulum/Intermediate Compartment of NT2N Cells , 1997, The Journal of cell biology.

[31]  P. Greengard,et al.  Generation of Alzheimer beta-amyloid protein in the trans-Golgi network in the apparent absence of vesicle formation. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[32]  D. Mann,et al.  Presence of soluble amyloid β–peptide precedes amyloid plaque formation in Down's syndrome , 1996, Nature Medicine.

[33]  S. Squazzo,et al.  Evidence that production and release of amyloid beta-protein involves the endocytic pathway. , 1994, The Journal of biological chemistry.

[34]  M. Zerial,et al.  The involvement of the small GTP-binding protein Rab5a in neuronal endocytosis , 1994, Neuron.

[35]  D. Selkoe,et al.  Normal Cellular Processing of the β‐Amyloid Precursor Protein Results in the Secretion of the Amyloid β Peptide and Related Molecules a , 1993 .

[36]  S. Mirra,et al.  Making the diagnosis of Alzheimer's disease. A primer for practicing pathologists. , 1993, Archives of pathology & laboratory medicine.

[37]  P. Greengard,et al.  Identification of the Alzheimer beta/A4 amyloid precursor protein in clathrin-coated vesicles purified from PC12 cells. , 1993, The Journal of biological chemistry.

[38]  Jean-Luc Galzi,et al.  Mutations in the channel domain of a neuronal nicotinic receptor convert ion selectivity from cationic to anionic , 1992, Nature.

[39]  Kai Simons,et al.  The small GTPase rab5 functions as a regulatory factor in the early endocytic pathway , 1992, Cell.

[40]  D. Selkoe,et al.  Targeting of cell-surface β-amyloid precursor protein to lysosomes: alternative processing into amyloid-bearing fragments , 1992, Nature.

[41]  S. M. Sumi,et al.  The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) , 1991, Neurology.

[42]  L. Cork.  Neuropathology of Down syndrome and Alzheimer disease. , 2005, American journal of medical genetics. Supplement.

[43]  K. Figura,et al.  Mannose 6‐phosphate receptor dependent secretion of lysosomal enzymes. , 1990, The EMBO journal.

[44]  M. Zerial,et al.  Localization of low molecular weight GTP binding proteins to exocytic and endocytic compartments , 1990, Cell.

[45]  E. Bird,et al.  Lysosomal proteinase antigens are prominently localized within senile plaques of Alzheimer's disease: evidence for a neuronal origin , 1990, Brain Research.

[46]  R. Mohs,et al.  Consortium to establish a registry for Alzheimer's disease (CERAD) clinical and neuropsychological assessment of Alzheimer's disease. , 2002, Psychopharmacology bulletin.

[47]  P. Yates,et al.  THE TOPOGRAPHY OF PLAQUES AND TANGLES IN DOWN'S SYNDROME PATIENTS OF DIFFERENT AGES , 1986, Neuropathology and applied neurobiology.

[48]  H. Wiśniewski,et al.  Occurrence of neuropathological changes and dementia of Alzheimer's disease in Down's syndrome , 1985, Annals of neurology.