Aging, gender and APOE isotype modulate metabolism of Alzheimer's Aβ peptides and F2‐isoprostanes in the absence of detectable amyloid deposits
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D. Holtzman | T. Montine | R. Martins | P. Davies | M. Ehrlich | C. Ouimet | S. Gandy | S. Schmidt | Eugene Laska | P. Mathews | Jonathan D. Smith | R. Nixon | L. Walker | C. Bisgaier | S. Petanceska | W. Lipinski | M. Callahan | Jun Yao | C. A. Parker | B. A. Turner
[1] J. Shioi,et al. Cyclooxygenase (COX)-2 and COX-1 Potentiate β-Amyloid Peptide Generation through Mechanisms That Involve γ-Secretase Activity* , 2003, Journal of Biological Chemistry.
[2] J. Buxbaum,et al. Molecular and Cellular Basis for Anti-Amyloid Therapy in Alzheimer Disease , 2003, Alzheimer disease and associated disorders.
[3] S. Gandy. Molecular basis for anti-amyloid therapy in the prevention and treatment of Alzheimer’s disease , 2002, Neurobiology of Aging.
[4] R. Rozmahel,et al. Alleles at the Nicastrin locus modify presenilin 1- deficiency phenotype , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[5] M. Mercken,et al. Calpain Activity Regulates the Cell Surface Distribution of Amyloid Precursor Protein , 2002, The Journal of Biological Chemistry.
[6] T. Montine,et al. Prostaglandin H2 (PGH2) accelerates formation of amyloid β1−42 oligomers , 2002, Journal of neurochemistry.
[7] T. Montine,et al. Peripheral F2‐isoprostanes and F4‐neuroprostanes are not increased in Alzheimer's disease , 2002, Annals of neurology.
[8] S. Arlt,et al. Lipid peroxidation in neurodegeneration: new insights into Alzheimer's disease , 2002, Current opinion in lipidology.
[9] R. Rozmahel,et al. Normal brain development in PS1 hypomorphic mice with markedly reduced γ-secretase cleavage of βAPP , 2002, Neurobiology of Aging.
[10] T. Montine,et al. Interactions between Apolipoprotein E Gene and Dietary α-Tocopherol Influence Cerebral Oxidative Damage in Aged Mice , 2001, The Journal of Neuroscience.
[11] D. Holtzman,et al. Behavioral Phenotyping of GFAP-ApoE3 and -ApoE4 Transgenic Mice: ApoE4 Mice Show Profound Working Memory Impairments in the Absence of Alzheimer's-like Neuropathology , 2001, Experimental Neurology.
[12] Virginia M. Y. Lee,et al. Increased Lipid Peroxidation Precedes Amyloid Plaque Formation in an Animal Model of Alzheimer Amyloidosis , 2001, The Journal of Neuroscience.
[13] J. Trojanowski,et al. Increased 8,12‐iso‐iPF2α‐VI in Alzheimer's disease: Correlation of a noninvasive index of lipid peroxidation with disease severity , 2000, Annals of neurology.
[14] D. Praticò,et al. Oxidative injury in diseases of the central nervous system: focus on Alzheimer's disease. , 2000, The American journal of medicine.
[15] S. Gandy,et al. Ovariectomy and 17β-estradiol modulate the levels of Alzheimer’s amyloid β peptides in brain , 2000, Neurology.
[16] A. Fagan,et al. Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[17] D. Praticò. F(2)-isoprostanes: sensitive and specific non-invasive indices of lipid peroxidation in vivo. , 1999, Atherosclerosis.
[18] T. Montine,et al. Elevated CSF prostaglandin E2 levels in patients with probable AD. , 1999, Neurology.
[19] D. Praticò,et al. Brains of Aged Apolipoprotein E‐Deficient Mice Have Increased Levels of F2‐Isoprostanes, In Vivo Markers of Lipid Peroxidation , 1999, Journal of neurochemistry.
[20] E. Masliah,et al. Synaptic alterations in apolipoprotein E knockout mice , 1999, Neuroscience.
[21] M. Jung,et al. Synaptotagmin and synaptic transmission alterations in apolipoprotein E-deficient mice , 1999, Progress in Neuro-Psychopharmacology and Biological Psychiatry.
[22] T. Montine,et al. Increased CSF F2-isoprostane concentration in probable AD , 1999, Neurology.
[23] J. Trojanowski,et al. Increased F2‐isoprostanes in Alzheimer's disease: evidence for enhanced lipid peroxidation in vivo , 1998, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[24] A. Fagan,et al. Evidence for Normal Aging of the Septo-Hippocampal Cholinergic System in apoE (−/−) Mice but Impaired Clearance of Axonal Degeneration Products Following Injury , 1998, Experimental Neurology.
[25] D. Michaelson,et al. Specific neurochemical derangements of brain projecting neurons in apolipoprotein E-deficient mice , 1997, Neuroscience Letters.
[26] A. Roses,et al. Age-related congophilic inclusions in the brains of apolipoprotein E-deficient mice , 1997, Neuroscience.
[27] Jonathan D. Smith,et al. Apolipoprotein E allele–specific antioxidant activity and effects on cytotoxicity by oxidative insults and β–amyloid peptides , 1996, Nature Genetics.
[28] A. Roses,et al. Neurodegeneration in the Central Nervous System of apoE-Deficient Mice , 1995, Experimental Neurology.
[29] M. Mattson,et al. A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[30] J. Growdon,et al. Treatment for Alzheimer's disease? , 1992, The New England journal of medicine.
[31] N. Maeda,et al. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. , 1992, Science.
[32] E. Rubin,et al. Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells , 1992, Cell.
[33] K. Beyreuther,et al. Amyloidogenicity of beta A4 and beta A4-bearing amyloid protein precursor fragments by metal-catalyzed oxidation. , 1992, The Journal of biological chemistry.
[34] W. Markesbery,et al. Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[35] B. Trapp,et al. Deposits of amyloid beta protein in the central nervous system of transgenic mice. , 1991, Science.
[36] D. Price,et al. Conservation of brain amyloid proteins in aged mammals and humans with Alzheimer's disease. , 1987, Science.
[37] INTERNATIONAL SOCIETY FOR NEUROCHEMISTRY , 1976 .
[38] F. Fremont‐Smith,et al. The cerebrospinal fluid , 1938 .
[39] J. Shioi,et al. Cyclooxygenase (COX)-2 and COX-1 potentiate beta-amyloid peptide generation through mechanisms that involve gamma-secretase activity. , 2003, The Journal of biological chemistry.
[40] R. Rozmahel,et al. Normal brain development in PS1 hypomorphic mice with markedly reduced gamma-secretase cleavage of betaAPP. , 2002, Neurobiology of aging.
[41] T. Montine,et al. Quantification of F-ring and D-/E-ring isoprostanes and neuroprostanes in Alzheimer's disease. , 2001, Advances in experimental medicine and biology.
[42] T. Montine,et al. Cerebrospinal Fluid Aβ42, Tau, and F2-Isoprostane Concentrations in Patients With Alzheimer Disease, Other Dementias, and in Age-Matched Controls , 2001 .
[43] D. Holtzman. Role of apoe/Abeta interactions in the pathogenesis of Alzheimer's disease and cerebral amyloid angiopathy. , 2001, Journal of molecular neuroscience : MN.
[44] S. Gandy,et al. Ovariectomy and 17beta-estradiol modulate the levels of Alzheimer's amyloid beta peptides in brain. , 2000, Neurology.
[45] R. Martins,et al. Plasma F2-isoprostane levels are increased in Alzheimer's disease: evidence of increased oxidative stress in vivo , 1999 .
[46] D. Price,et al. Age-associated inclusions in normal and transgenic mouse brain. , 1992, Science.
[47] B. Trapp,et al. Age-associated inclusions in normal and transgenic mouse brain. , 1992, Science.
[48] M. Spiegel-Adolf. Cerebrospinal fluid. , 1965, Progress in neurology and psychiatry.