Oxygen-free radicals and amyloidosis in alzheimer's disease: Is there a connection?
暂无分享,去创建一个
[1] L. Butcher,et al. Involvement of free oxygen radicals in β-amyloidosis: An hypothesis , 1994, Neurobiology of Aging.
[2] Carl W. Cotman,et al. Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[3] L. Thal,et al. Secretion of β-amyloid precursor protein cleaved at the amino terminus of the β-amyloid peptide , 1993, Nature.
[4] N. Robakis,et al. An Alternative Secretase Cleavage Produces Soluble Alzheimer Amyloid Precursor Protein Containing a Potentially Amyloidogenic Sequence , 1992, Journal of neurochemistry.
[5] S. Estus,et al. Production of the Alzheimer amyloid beta protein by normal proteolytic processing. , 1992, Science.
[6] D. Selkoe,et al. Amyloid β-peptide is produced by cultured cells during normal metabolism , 1992, Nature.
[7] D. Stephenson,et al. Implants containing β-amyloid protein are not neurotoxic to young and old rat brain , 1992, Neurobiology of Aging.
[8] B. Winblad,et al. A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloid , 1992, Nature Genetics.
[9] C. Barrow,et al. Solution conformations and aggregational properties of synthetic amyloid beta-peptides of Alzheimer's disease. Analysis of circular dichroism spectra. , 1992, Journal of molecular biology.
[10] Bradley T. Hyman,et al. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease , 1992, Neurology.
[11] N. Robakis,et al. Immunohistochemical evidence of antioxidant stress in Alzheimer's disease , 1992 .
[12] C. Cotman,et al. Assembly and aggregation properties of synthetic Alzheimer's A4/beta amyloid peptide analogs. , 1992, The Journal of biological chemistry.
[13] 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.
[14] N. Robakis,et al. Exact cleavage site of Alzheimer amyloid precursor in neuronal PC-12 cells , 1991, Neuroscience Letters.
[15] S. Papasozomenos,et al. Altered phosphorylation of tau protein in heat-shocked rats and patients with Alzheimer disease. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[16] R. Krumlauf,et al. Introduction of a subtle mutation into the Hox-2.6 locus in embryonic stem cells , 1991, Nature.
[17] D. Drachman,et al. Expression of heat shock proteins in Alzheimer's disease , 1991, Neurology.
[18] M. Pericak-Vance,et al. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease , 1991, Nature.
[19] M. Chalfie,et al. The mec-4 gene is a member of a family of Caenorhabditis elegans genes that can mutate to induce neuronal degeneration , 1991, Nature.
[20] E. Masliah,et al. Diffuse plaques do not accentuate synapse loss in Alzheimer's disease. , 1990, The American journal of pathology.
[21] D. Kirschner,et al. Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. , 1990, Science.
[22] P. Crino,et al. Involvement of free radicals in dementia of the Alzheimer type: A hypothesis , 1990, Neurobiology of Aging.
[23] C. Bouras,et al. Down patients: Extracellular preamyloid deposits precede neuritic degeneration and senile plaques , 1989, Neuroscience Letters.
[24] L. Wolfson,et al. Clinico‐pathologic studies in dementia , 1988, Neurology.
[25] Y. Ihara,et al. Ubiquitin is a component of paired helical filaments in Alzheimer's disease. , 1987, Science.
[26] D. Mann,et al. Changes in nerve cells of the nucleus basalis of Meynert in Alzheimer's disease and their relationship to ageing and to the accumulation of lipofuscin pigment , 1984, Mechanisms of Ageing and Development.
[27] A. Fotheringham,et al. The effect of lipofuscin on cellular function , 1983, Mechanisms of Ageing and Development.
[28] M. Best-Belpomme,et al. The possible role of the superoxide ion in the induction of heat-shock and specific proteins in aerobic Drosophila cells during return to normoxia after a period of anaerobiosis. , 1983, Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire.
[29] D. Harman,et al. Free radical theory of aging: effect of free radical reaction inhibitors on the mortality rate of male LAF mice. , 1968, Journal of gerontology.
[30] M. Pappolla,et al. The "normal" brain. "Abnormal" ubiquitinilated deposits highlight an age-related protein change. , 1989, The American journal of pathology.
[31] S. Lange,et al. The normal brain , 1989 .
[32] S. Sharma,et al. Reversibility of lipofuscin accumulation caused by protein malnutrition in the motor cortex of squirrel monkeys, Saimiri scireus. , 1977, Acta histochemica.