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The Alzheimer's disease beta-amyloid peptide (Abeta) is produced by excision from the type 1 integral membrane glycoprotein amyloid precursor protein (APP) by the sequential actions of beta- and then gamma-secretases. Here we report that Asp 2, a novel transmembrane aspartic protease, has the key activities expected of beta-secretase. Transient expression(More)
The purpose of this report is to convey the findings of the DTI – funded International Technology Service Mission on North American Best Practice in Mobile Entertainment.The mission investigated a broad range of North American companies involved in the development of mobile content including mobile game developers and publishers, as well as mobile service(More)
Sequential proteolytic processing of the Amyloid Precursor Protein (APP) by beta- and gamma-secretases generates the 4-kDa amyloid (A beta) peptide, a key component of the amyloid plaques seen in Alzheimer's disease (AD). We and others have recently reported the identification and characterisation of an aspartic proteinase, Asp2 (BACE), as beta-secretase.(More)
The deposition of beta-amyloid (Abeta) in the brain is a neuropathological feature of Alzheimer's disease. Abeta is cleaved from its precursor protein (APP) by processing at its N and C termini by enzymes known as beta- and gamma-secretases,respectively. The identity of these enzymes has been elusive but the search for the N-terminal secretase might have(More)
Peptide aldehyde inhibitors of the chymotrypsin-like activity of the proteasome (CLIP) such as N-acetyl-Leu-Leu-Nle-H (or ALLN) have been shown previously to inhibit the secretion of beta-amyloid peptide (A beta) from cells. To evaluate more fully the role of the proteasome in this process, we have tested the effects on A beta formation of a much wider(More)
The discovery of the PS proteins, the complexities of their biochemistry and their potential involvement in signalling pathways and in apoptosis have galvanized research into AD. To date, the aspect of the functionality of the PSs most relevant to the pathology of AD is the effect of PS FAD mutants to increase the proportion of A beta 42 produced from(More)
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