Occurrence and co-localization of amyloid β-protein and apolipoprotein E in perivascular drainage channels of wild-type and APP-transgenic mice

[1]  D. Dickson,et al.  Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders: Dickson/Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders , 2011 .

[2]  D. Dickson,et al.  Induction of vascular amyloidosis-β by oxidative stress depends on APOE genotype , 2006, Neurobiology of Aging.

[3]  H. Braak,et al.  Apolipoprotein E co-localizes with newly formed amyloid β-protein (Aβ) deposits lacking immunoreactivity against N-terminal epitopes of Aβ in a genotype-dependent manner , 2005, Acta Neuropathologica.

[4]  S. Paul,et al.  Cognitive impairment in PDAPP mice depends on ApoE and ACT-catalyzed amyloid formation , 2004, Neurobiology of Aging.

[5]  Thomas Wisniewski,et al.  A synthetic peptide blocking the apolipoprotein E/β-amyloid binding mitigates β-amyloid toxicity and fibril formation in vitro and reduces β-amyloid plaques in transgenic mice , 2004 .

[6]  S. Paul,et al.  Apolipoprotein E promotes astrocyte colocalization and degradation of deposited amyloid-β peptides , 2004, Nature Medicine.

[7]  J. Frackowiak,et al.  Secretion and Accumulation of Aβ by Brain Vascular Smooth Muscle Cells from AβPP‐Swedish Transgenic Mice , 2003 .

[8]  L. Hersh,et al.  Amyloid-β peptide levels in brain are inversely correlated with insulysin activity levels in vivo , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[9]  T. Iwatsubo.  Molecular pathogenesis of Alzheimer's disease. , 2003, Internal medicine.

[10]  P. Greengard,et al.  Intraneuronal Alzheimer abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology. , 2002, The American journal of pathology.

[11]  M. Salto‐Tellez,et al.  AFP+, ESC‐Derived Cells Engraft and Differentiate into Hepatocytes in Vivo , 2002, Stem cells.

[12]  H. Braak,et al.  Two Types of Sporadic Cerebral Amyloid Angiopathy , 2002, Journal of neuropathology and experimental neurology.

[13]  T. Saido,et al.  Reply to: 'Clearance of amyloid β-peptide from brain: transport or metabolism?' , 2000, Nature Medicine.

[14]  L. Thal,et al.  Association between severe cerebral amyloid angiopathy and cerebrovascular lesions in Alzheimer disease is not a spurious one attributable to apolipoprotein E4. , 2000, Archives of neurology.

[15]  T. Saido,et al.  Identification of the major Aβ1–42-degrading catabolic pathway in brain parenchyma: Suppression leads to biochemical and pathological deposition , 2000, Nature Medicine.

[16]  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.

[17]  C. Duyckaerts,et al.  Neuropathological aspects of Alzheimer disease , 1999 .

[18]  M. Tabaton,et al.  Opposite roles of apolipoprotein E in normal brains and in Alzheimer's disease. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[19]  R. Weller.  Pathology of Cerebrospinal Fluid and Interstitial Fluid of the CNS: Significance for Alzheimer Disease, Prion Disorders and Multiple Sclerosis , 1998, Journal of neuropathology and experimental neurology.

[20]  Yu-Min Kuo,et al.  Cerebral amyloid angiopathy: amyloid beta accumulates in putative interstitial fluid drainage pathways in Alzheimer's disease. , 1998, The American journal of pathology.

[21]  Y. Ihara,et al.  Diffuse plaques associated with astroglial amyloid β protein, possibly showing a disappearing stage of senile plaques , 1998, Acta Neuropathologica.

[22]  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.

[23]  S. Paul,et al.  Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition , 1997, Nature Genetics.

[24]  R O Weller,et al.  Perivascular spaces in the basal ganglia of the human brain: their relationship to lacunes , 1997, Journal of anatomy.

[25]  Y. Ihara,et al.  Intracellular Generation and Accumulation of Amyloid β-Peptide Terminating at Amino Acid 42* , 1997, The Journal of Biological Chemistry.

[26]  H. Wiśniewski,et al.  Accumulation of Alzheimer Amyloid‐β Peptide in Cultured Myocytes is Enhanced by Serum and Reduced by Cerebrospinal Fluid , 1997, Journal of neuropathology and experimental neurology.

[27]  S. Younkin,et al.  Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.

[28]  D. Selkoe,et al.  Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation , 1996, Neurobiology of Disease.

[29]  C. Wernstedt,et al.  Characterization of stable complexes involving apolipoprotein E and the amyloid β peptide in Alzheimer's disease brain , 1995, Neuron.

[30]  L. Mucke,et al.  Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein , 1995, Nature.

[31]  H. Wiśniewski,et al.  Non‐Fibrillar β‐Amyloid Protein is Associated with Smooth Muscle Cells of Vessel Walls in Alzheimer Disease , 1994, Journal of neuropathology and experimental neurology.

[32]  A D Roses,et al.  Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[33]  M. Pericak-Vance,et al.  Binding of human apolipoprotein E to synthetic amyloid beta peptide: isoform-specific effects and implications for late-onset Alzheimer disease. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[34]  E. Otomo,et al.  Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease , 1991, Brain Research.

[35]  J. Taylor,et al.  Apolipoprotein E associated with astrocytic glia of the central nervous system and with nonmyelinating glia of the peripheral nervous system. , 1985, The Journal of clinical investigation.

[36]  C. Masters,et al.  Amyloid plaque core protein in Alzheimer disease and Down syndrome. , 1985, Proceedings of the National Academy of Sciences of the United States of America.

[37]  G. Glenner.  Amyloid deposits and amyloidosis. The beta-fibrilloses (first of two parts). , 1980, The New England journal of medicine.

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

[39]  T. V. Van Dooren,et al.  Neuronal or glial expression of human apolipoprotein e4 affects parenchymal and vascular amyloid pathology differentially in different brain regions of double- and triple-transgenic mice. , 2006, The American journal of pathology.

[40]  E. Zhang,et al.  Directional and compartmentalised drainage of interstitial fluid and cerebrospinal fluid from the rat brain , 2004, Acta Neuropathologica.

[41]  H. Braak,et al.  Amyloid β-protein (Aβ)-containing astrocytes are located preferentially near N-terminal-truncated Aβ deposits in the human entorhinal cortex , 2000, Acta Neuropathologica.