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Amyloid-beta (Abeta) specifically bound purified catalase with high affinity and inhibited catalase breakdown of H(2)O(2). The Abeta-induced catalase inhibition involved formation of the inactive catalase Compound II and was reversible. Catalase<-->Abeta interactions provide rapid functional assays for the cytotoxic domain of Abeta and suggest a mechanism(More)
The amyloid-beta (Abeta) peptide has been implicated in the pathology of Alzheimer's disease (AD). Using an antisense peptide approach a novel interaction between Abeta and the human cdc2 kinase was identified. The Abeta 1-42, 1-40 and 25-35 peptides were shown to be substrates for the cdc2 kinase and phosphorylated on the Serine 26 residue. Phosphorylated(More)
Cannabinoid receptor agonists including anandamide and noladin either have recently been suggested to exhibit neuroprotective properties. The amyloid-beta (Abeta) peptide is thought to be responsible for the neurodegenerative changes associated with Alzheimer's disease pathology. This study characterizes the effects of anandamide and noladin ether on the(More)
Hydrogen peroxide (H(2)O(2)) is a stable, uncharged and freely diffusable reactive oxygen species (ROS) and second messenger. The generation of H(2)O(2) in the brain is relatively high because of the high oxygen consumption in the tissue. Alzheimer's disease is a neurodegenerative disorder characterised by the appearance of amyloid-beta (Abeta)-containing(More)
The pyrogenic interferon inducer polyinosinic:polycytidylic acid (Poly I:C) was shown to activate the rabbit hypothalamo-pituitary-adrenocortical (HPA) axis in vivo. The immunoreactive cortisol response to Poly I:C (2.5 micrograms/kg) was shown to have a corticotrophin-releasing factor-41 (CRF-41)-dependent component which was abolished by peripheral(More)
Amyloid-beta, (Abeta) is a cytotoxic peptide implicated in the pathology of Alzheimers disease. The antioxidant enzyme catalase has been suggested to protect against Abeta cytotoxicity in both neuronal and non-neuronal cell types. Inhibition of endogenous catalase using 3-amino-1,2,4-triazole (3AT) in neuronal (NT-2) and myeloma (SP2/0-Ag-14) cell lines(More)
The regulatory region of the neuronal nicotinic acetylcholine (nACh) receptor alpha 2 subunit gene is activated by the Brn-3b POU family transcription factor but not by the closely related factors Brn-3a and Brn-3c. This pattern of regulation has not previously been observed for other neuronally expressed genes, several of which, such as those encoding(More)
1. The actions of peripheral corticotrophin-releasing factor-41 (CRF-41) on the febrile responses of conscious rabbits induced by peripherally administered polyinosinic.polycytidylic acid (poly(I).poly(C)) have been studied using a CRF-41 receptor antagonist (alpha-helical CRF(9-41) and anti-CRF-41 monoclonal antibodies. 2. Temperature responses were(More)
Murine monoclonal antibodies against human/rat corticotrophin-releasing factor-41 (CRF-41) were produced and characterized for use in the immunological and biological characterization of CRF-41. Spleen cells from BALB/c mice immunized with CRF-41 conjugated to bovine gamma-globulin were fused with a BALB/c-derived non-secretor X-63 myeloma line. Hybridomas(More)
The concentration of immunoreactive, placentally derived CRH is increased in the peripheral circulation during the third trimester of human pregnancy. However, the function of this placental CRH is entirely unknown. A number of observations have led us to believe that CRH might influence myometrial contractility and, hence, parturition via specific receptor(More)