Altered plasma cytokine levels in Alzheimer's disease: correlation with the disease progression.
暂无分享,去创建一个
F. Stivala | R. Imbesi | M. Di Rosa | F Stivala | M. Motta | L. Malaguarnera | M. Rosa | M Motta | R Imbesi | M Di Rosa | L Malaguarnera | M. Motta
[1] R. Comolli,et al. Decrease of TGF-β1 plasma levels and increase of nitric oxide synthase activity in leukocytes as potential biomarkers of Alzheimer's disease , 2002, Experimental Gerontology.
[2] W. Fridman,et al. Interleukin-18: biological properties and clinical implications. , 2000, European cytokine network.
[3] T. Bártfai,et al. Interleukin-18 null mice show diminished microglial activation and reduced dopaminergic neuron loss following acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment , 2004, Neuroscience.
[4] D. Kögel,et al. TGF-β1 activates two distinct type I receptors in neurons , 2005, The Journal of Cell Biology.
[5] D. Gambi,et al. Treatment with an acetylcholinesterase inhibitor in Alzheimer patients modulates the expression and production of the pro-inflammatory and anti-inflammatory cytokines , 2004, Journal of Neuroimmunology.
[6] C. Cotman,et al. Transforming growth factor-β1 is in plaques in Alzheimer and Down pathologies , 1993 .
[7] T. Joh,et al. Cultures of astrocytes and microglia express interleukin 18. , 1999, Brain research. Molecular brain research.
[8] H. Lassmann,et al. APP peptides stimulate lymphocyte proliferation in normals, but not in patients with Alzheimer's Disease , 1996, Neurobiology of Aging.
[9] J. Aldenhoff,et al. The calcium response of human T lymphocytes is decreased in aging but increased in Alzheimer’s dementia , 1999, Biological Psychiatry.
[10] V. Haroutunian,et al. Cytokine gene expression as a function of the clinical progression of Alzheimer disease dementia. , 2000, Archives of neurology.
[11] B. Winblad,et al. Neuronal expression of caspase-1 immunoreactivity in the rat central nervous system , 2004, Journal of Neuroimmunology.
[12] Anders Wallin,et al. Increased intrathecal levels of the angiogenic factors VEGF and TGF-β in Alzheimer’s disease and vascular dementia , 2002, Neurobiology of Aging.
[13] E. Mackenzie,et al. Transforming Growth Factor-β1 Potentiates Amyloid-β Generation in Astrocytes and in Transgenic Mice* , 2003, The Journal of Biological Chemistry.
[14] N. Bannert,et al. Cutting Edge: CD4 Is Not Required for the Functional Activity of IL-161 , 2000, The Journal of Immunology.
[15] F. Paoletti,et al. Increased plasma levels of soluble CD40, together with the decrease of TGFβ1, as possible differential markers of Alzheimer disease , 2004, Experimental Gerontology.
[16] Y. Stern,et al. Hospitalization and Alzheimer's disease: results from a community-based study. , 1999, The journals of gerontology. Series A, Biological sciences and medical sciences.
[17] M. Malaguarnera,et al. Interleukin‐18 and transforming growth factor‐beta 1 plasma levels in Alzheimer’s disease and vascular dementia , 2006, Neuropathology : official journal of the Japanese Society of Neuropathology.
[18] P. Mecocci,et al. Oxidative damage to DNA in lymphocytes from AD patients , 1998, Neurology.
[19] Lawrence Da. Transforming growth factor-beta: a general review. , 1996, European cytokine network.
[20] F. Nicoletti,et al. Chitotriosidase and inflammatory mediator levels in Alzheimer's disease and cerebrovascular dementia , 2006, The European journal of neuroscience.
[21] K. Blennow,et al. Intrathecal inflammation precedes development of Alzheimer’s disease , 2003, Journal of neurology, neurosurgery, and psychiatry.
[22] J Marshall,et al. Cerebral blood flow in dementia. , 1975, Archives of neurology.
[23] M. Folstein,et al. Clinical diagnosis of Alzheimer's disease , 1984, Neurology.
[24] Elisabeth Kapaki,et al. Interleukin-12 is reduced in cerebrospinal fluid of patients with Alzheimer's disease and frontotemporal dementia , 2006, Journal of the Neurological Sciences.
[25] A. Thomson. The cytokine handbook , 1994 .
[26] P. Lipton,et al. Ischemic cell death in brain neurons. , 1999, Physiological reviews.
[27] K. Blennow,et al. Increased cerebrospinal fluid levels of transforming growth factor-β1 in Alzheimer’s disease , 2004, Neuroscience Letters.
[28] J. Schwab,et al. Human focal cerebral infarctions induce differential lesional interleukin-16 (IL-16) expression confined to infiltrating granulocytes, CD8+ T-lymphocytes and activated microglia/macrophages , 2001, Journal of Neuroimmunology.
[29] C D Marsden,et al. Mini-mental state examination in neurological patients. , 1984, Journal of neurology, neurosurgery, and psychiatry.
[30] G. Annoni,et al. Increased plasma levels of interleukin-1, interleukin-6 and α-1-antichymotrypsin in patients with Alzheimer's disease: peripheral inflammation or signals from the brain? , 2000, Journal of Neuroimmunology.
[31] F. Giubilei,et al. T Cell Response to Amyloid-β and to Mitochondrial Antigens in Alzheimer’s Disease , 2003, Dementia and Geriatric Cognitive Disorders.
[32] P. Mcgeer,et al. The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases , 1995, Brain Research Reviews.
[33] R. Cacabelos,et al. Characterization of cytokine production, screening of lymphocyte subset patterns and in vitro apoptosis in healthy and Alzheimer's Disease (AD) individuals , 1999, Journal of Neuroimmunology.
[34] H. Schluesener,et al. Leukocyte chemotactic factor, a natural ligand to CD4, is expressed by lymphocytes and microglial cells of the MS plaque , 1996, Journal of neuroscience research.
[35] D. Feinstein,et al. Effect of anti-inflammatory agents on transforming growth factor beta over-expressing mouse brains: a model revised , 2004, Journal of Neuroinflammation.
[36] A. J. Valente,et al. Interleukin-18 induces human cardiac endothelial cell death via a novel signaling pathway involving NF-kappaB-dependent PTEN activation. , 2006, Biochemical and biophysical research communications.
[37] N. Rothwell,et al. Interleukin‐18 induces expression and release of cytokines from murine glial cells: interactions with interleukin‐1β , 2003, Journal of neurochemistry.
[38] L. Mucke,et al. Amyloidogenic role of cytokine TGF-β1 in transgenic mice and in Alzheimer's disease , 1997, Nature.
[39] K. Suk,et al. Regulation of IL-18 production by IFN gamma and PGE2 in mouse microglial cells: involvement of NF-kB pathway in the regulatory processes. , 2001, Immunology letters.
[40] Dc Washington. Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. , 1994 .
[41] J. Cummings,et al. Telomere shortening in T cells correlates with Alzheimer’s disease status , 2003, Neurobiology of Aging.
[42] H. Okamura,et al. Cloning of a new cytokine that induces IFN-γ production by T cells , 1995, Nature.
[43] N. Rothwell,et al. Detection of the interleukin 18 family in rat brain by RT-PCR. , 2000, Brain research. Molecular brain research.
[44] R. Mrak,et al. Welcome to the Journal of Neuroinflammation! , 2004, Journal of Neuroinflammation.