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Beta amyloid

Dodart JC, Meziaue H, Mathis C, Bales KR, Paul SM, Uugerer A (1999) Behavioral disturbauces iu transgeuic mice overexpressiug the V717E beta-amyloid precursor proteiu. Behav Neurosd 113 982-990... [Pg.292]

Saez ET, Pehar M, Vargas MR, Barbeito L, Maccioni RB (2006) Production of nerve growth factor by beta-amyloid-stimulated astrocytes induces p75NTR-dependent tau hyperphosphorylation in cultured hippocampal neurons. J Neurosci Res 84 1098-1106 Sala C, Roussignol G, Meldolesi J, Fagni L (2005) Key role of the postsynaptic density scaffold proteins Shank and Homer in the functional architecture of Ca homeostasis at dendritic spines in hippocampal neurons. J Neurosci 25 4587 592 Santello M, Volterra A (2008) Synaptic modulation by astrocytes via Ca(2-l-)-dependent glutamate release. Neuroscience 158 253-9... [Pg.298]

ROTH A, scHAFFNER w and BERTEL c (1999) Phytoestrogen kaempferol (3,4, 5,7-tetrahydroxyflavone) protects PC 12 andT47D cells from beta-amyloid-induced toxicity. JNeurosci Res. 57 (3) 399-404. [Pg.219]

Park, S.Y. and Kim, D.S., Discovery of natural products from Curcuma longa that protect cells from beta-amyloid insult a drug discovery effort against Alzheimer s disease, J. Nat. Prod., 65, 1227, 2002. [Pg.343]

Evidence for a neuroimmunological involvement in Alzheimer s disease is accumulating. Activation of the complement cascade by beta amyloid (Rogers et al., 1992), the recruitment, proliferation and activation of microglia in intimate juxtaposition to the senile plaques (Davis et al., 1992), and the increased synthesis of microglia-derived pro-inflammatory cytokine interleukin-1 (Griffin et al., 1989) is indicative of a chronic inflam-... [Pg.253]

Bihel, F. Quelever, G. Lelouard, H. Petit, A. Alves de Costa, C. Pourqie, O. Checler, F. Thellend, A. Pierre, P Kraus, J.-L. Synthesis of new 3-alkoxy-7-amino-4-chloro-isocoumarin derivatives as new beta-amyloid peptide production inhibitors and their activities on various classes of protease. Bioorg. Med. Chem. 2003, 11, 3141-3152. [Pg.382]

Han H, Weinreb PH, Lansbury PT Jr. The core Alzheimer s peptide NAC forms amyloid fibrils which seed and are seeded by beta-amyloid is NAC a common trigger or target in neurodegenerative disease Chem Biol 1995 2 163-169. [Pg.273]

Burdick D, Soreghan B, Kwon M, Kosmoski J, Rnauer M, Henschen A, Yates J, Cotman C, Glabe C. Assembly and aggregation properties of synthetic Alzheimer s A4/beta amyloid peptide analogs. J Biol Chem 1992 267 546-554. [Pg.276]

Shen CL, Scott GL, Merchant F, Murphy RM. Light scattering analysis of fibril growth from the amino-terminal fragment beta(l-28) of beta-amyloid peptide. Biophys J 1993 65 2383-2395. [Pg.277]

Tomski SJ, Murphy RM. Kinetics of aggregation of synthetic beta-amyloid peptide. Arch Biochem Biophys 1992 294 630-638. [Pg.277]

Kowalewski T, Holtzman DM. In situ atomic force microscopy study of Alzheimer s beta-amyloid peptide on different substrates new insights into mechanism of beta-sheet formation. Proc Natl Acad USA 1999 96 3688-3693. [Pg.278]

Inouye H, Fraser PE, Kirschner DA. Structure of beta-crystalline assemblies formed by Alzheimer beta-amyloid protein analogues analysis by X-ray diffraction. Biophys J 1993 64 502-519. [Pg.278]

Naiki H, Nakakuki K. First-order kinetic model of Alzheimer s beta-amyloid fibril extension in vitro. Lab Invest 1996 74 374-383. [Pg.279]

Esler WP, Stimson ER, Ghilardi JR, Lu YA, Felix AM, Vinters HV, Mantyh PW, Lee JP, Maggio JE. Point substitution in the central hydrophobic cluster of a human beta-amyloid congener disrupts peptide folding and abolishes plaque competence. Biochemistry 1996 35 13914-13921. [Pg.279]

Dudek SM, Johnson GV. Transglutaminase facilitates the formation of polymers of the beta-amyloid peptide. Brain Res 1994 651 129-133. [Pg.279]

Pallitto MM, Ghanta J, Heizelman P, Kiessling LL, Murphy RM. Recognition sequence design for peptidyl modulators of beta-amyloid aggregation and toxicity. Biochemistry 1999 38 3570-3578. [Pg.279]

Ghanta J, Shen CL, Kiessling LL, Murphy RM. A strategy for designing inhibitors of beta-amyloid toxicity. J Biol Chem 1996 271 ... [Pg.280]

Howlett DR, Perry AE, Godfrey F, Swatton JE, Jennings KH, Spitzfaden C, Wadsworth H, Wood SJ, Markwell RE. Inhibition of fibril formation in beta-amyloid peptide by a novel series of benzofurans. Biochem J 1999 ... [Pg.280]

Wisniewski HM, Frackowiak J, Mazur Kolecka B. In vitro production of beta-amyloid in smooth muscle cells isolated from amylid angiopathy-affected vessels. Neurosci Lett 1995 183 120-123. [Pg.280]

Mullan M. Alzheimer s beta-amyloid vasoactivity identification of a novel beta-amyloid conformational intermediate. FEBS Lett 1998 436 445-448. [Pg.281]

Lorenzo A, Yankner BA. Beta-amyloid neurotoxicity requires fibril formation and is inhibited by Congo Red. Proc Natl Acad Sci USA 1994 91 12243-12247. [Pg.281]

Sadler II, Smith DW, Shearman MS, Ragan Cl, Tailor VJ, Pollack SJ. Sulphated compounds attenuate beta-amyloid toxicity by inhibiting its association with cells. Neuroreport 1995 7 49-53. [Pg.281]

Walker LC. Animal models of cerebral beta-amyloid angiopathy. Brain Res Brain Res Rev 1997 25 70-84. [Pg.281]

Howlett D, Cutler P, Heales S, Camilleri P. Hemin and related porphyrins inhibit beta-amyloid aggregation. FEBS Lett 1997 417 249-251. [Pg.282]

Selkoe, D. J. (1998). The cell biology of beta-amyloid precursor protein and presenilin in Alzheimer s disease. Trends Cell Biol. 8, 447-453. [Pg.122]

Khandogin J, Brooks CL III (2007) Linking folding with aggregation in Alzheimer s beta amyloid peptides. Proc Natl Acad Sci USA 104 16880-16885. [Pg.281]

The lack of zinc can also be a problem in biological systems and is responsible for disease states. For example, nitric oxide-dependent apoptosis can be induced in motor neurons by zinc-deficient SOD, and in some cases of amyotrophic lateral sclerosis, zinc-deficient SOD may participate in this type of oxidative mechanism involving nitric oxide.969 One form of hereditary human hair loss or alopecia was mapped to a specific gene and a mutation found in affected individuals. The gene encodes a single zinc finger transcription factor protein with restricted expression in the brain and skin.970 Zinc has been implicated in Alzheimer s via beta amyloid formation, and a role has been attributed for the cerebral zinc metabolism in the neuropathogenesis of Alzheimer s disease.971... [Pg.1233]

Dineley, K.T., Westerman, M., Bui, D., Bell, K., Ashe, K.H., Sweatt, J.D. Beta-amyloid activates the mitogen-activated protein kinase cascade via hippocampal alpha7 nicotinic acetylcholine receptors in vitro and in vivo mechanisms related to Alzheimer s disease. J. Neurosci. 21 4125, 2001. [Pg.36]

Strittmatter WJ, Saunders AM, Schmechel D, Pericak-Vance M, Enghild J, Salvesen GS and Roses AD (1993). Apolipoprotein E High-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proceedings of the National Academy of Science USA, 90, 1977-1981. [Pg.284]

Sunderland, T., Linker, G., Mirza, N. et al. Decreased beta-amyloid 1-42 and increased tau levels in cerebrospinal fluid of patients with Alzheimer disease. JAMA 289 2094-2103, 2003. [Pg.788]

Luo, Y., Bolon, B., Kahn, S. et al. Mice deficient in BACE1, the Alzheimer s beta-secretase, have normal phenotype and abolished beta-amyloid generation. Nature Neurosci. 4 231-232, 2001. [Pg.789]

Li, T., Ma, G., Cai, H. etal. Nicastrin is required for assembly of presenilin/gamma-secretase complexes to mediate notch signaling and for processing and trafficking of beta-amyloid precursor protein in mammals. /. Neurosci. 23 3272-3277, 2003. [Pg.789]

Capell, A., Steiner,H.,Romig,H. etal. Presenilin-1 differentially facilitates endoproteolysis of the beta-amyloid precursor protein and Notch. Nature Cell Biol. 2 205-211, 2000. [Pg.789]

Figure 17.5. The precursor molecule APP and the three different proteases a, (i, y secretase that are involved in the processing of APPto fS-amyloid peptide. The aberrant processing of the amyloid precursor protein (APP) leads to accumulation of beta-amyloid fragments, first as protofibrils and then as fibers that aggregate in the senile plaque structures. (See color insert.)... Figure 17.5. The precursor molecule APP and the three different proteases a, (i, y secretase that are involved in the processing of APPto fS-amyloid peptide. The aberrant processing of the amyloid precursor protein (APP) leads to accumulation of beta-amyloid fragments, first as protofibrils and then as fibers that aggregate in the senile plaque structures. (See color insert.)...
Balbach, J. J., Ishii, Y., Antzutkin, O. N., Leapman, R. D., Rizzo, N. W., Dyda, F., Reed,J., and Tycko, R. (2000). Amyloid fibril formation by A beta 16-22, a seven-residue fragment of the Alzheimer s beta-amyloid peptide, and structural characterization by solid state NMR. Biochemistry 39, 13748-13759. [Pg.14]

Benzinger, T. L., Gregory, D. M., Burkoth, T. S., Miller-Auer, H., Lynn, D. G., Botto, R. E., and Meredith, S. C. (1998). Propagating structure of Alzheimer s beta-amyloid (10-35) is parallel beta-sheet with residues in exact register. Proc. Natl. Acad. Sci. USA 95, 13407-13412. [Pg.14]


See other pages where Beta amyloid is mentioned: [Pg.292]    [Pg.292]    [Pg.293]    [Pg.295]    [Pg.372]    [Pg.151]    [Pg.253]    [Pg.103]    [Pg.167]    [Pg.359]    [Pg.365]    [Pg.333]   
See also in sourсe #XX -- [ Pg.294 ]

See also in sourсe #XX -- [ Pg.25 , Pg.26 , Pg.27 , Pg.28 , Pg.29 , Pg.30 , Pg.31 , Pg.32 , Pg.33 , Pg.34 , Pg.117 , Pg.118 ]




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