Society for Neuroscience Annual Meeting: Endocrepsin is BACE

CONFERENCE COVERAGE 1999-10-25 Conference Coverage At times the scene around this poster (240.11) was more like a football scrimmage or a rugby scrum than the normally genteel atmosphere associated with a scientific event. By the time I made my way to within sight of the poster, the pr

Soc for Neuroscience Ann Mtg: Proteasome Inhibition Boosts Aβ

CONFERENCE COVERAGE 1999-10-25 Conference Coverage Janet Johnston (240.16) presented a detailed study of the effect of proteasome and prolendopeptidase (PEP) inhibitors on Aβ production by SH SY 5Y human neuroblastoma cells stably transfected with SPA4CT (C99). Both the proteasome and

Society for Neuroscience Annual Meeting: APP Binds to Fibrillar Aβ

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Treatment of human cerebovascular smooth muscle (HCSM) cells with Aβ1-42 or AβQ22 (a mutant associated with hereditary cerebral hemorrhage with amyloidosis-Dutch type) leads to the formation of amyloid fibrils on the surface of HCSM ce

Society for Neuroscience Annual Meeting: Evidence for Additional Genetic Risk Factors for AD

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Papassotiropoulos (1201) began his presentation by reviewing the evidence for a role of cathepsin D, an aspartyl protease, in AD. Previous work has implicated catD as a secretase in the cleavage of APP. It is found in plaques and exhib

Society for Neuroscience Annual Meeting: Imaging Amyloid Plaques in the Living Mouse

CONFERENCE COVERAGE 1999-10-24 Conference Coverage One of the limitations in studying the pathogenic role of amyloid plaque deposition is the fact that conventional methods allow microscopic analysis only of postmortem tissue, which can provide only a single snapshot of a process that

Society for Neuroscience Annual Meeting: β-Secretase Further Confirmed

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Sukanto Sinha, departing from his abstract (122.1), described the purification and partial characterization of a novel 501 amino acid long aspartyl protease. The data were entirely consistent with the β-secretase activities reported by

Society for Neuroscience Annual Meeting: Another APP Secretase?

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Just when it appeared as though the mechanisms of the proteolytic processing of APP were finally becoming apparent, Andreas Weidemann presented an elegant study demonstrating the existence of a different processing event (122.2). Using

Soc for Neuroscience Ann Mtg: One γ-Secretase, Two Different Activities?

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Using difluoroketone peptidomimetics previously shown to reversibly inhibit γ-secretase activity in CHO cells, Michael Wolfe reported that increasing the bulkiness of the P1 substituent of these compounds increased their potency, thus,

Society for Neuroscience Annual Meeting: Caspase-mediate Production of Aβ

CONFERENCE COVERAGE 1999-10-24 Conference Coverage In testing the hypothesis that unscheduled cell death may alter APP processing, Andrea Le Blanc (122.4) provided compelling evidence that caspase 6 can directly cleave APP and cause an increase in Aβ levels in serum deprived human prim

Soc for Neuroscience Ann Mtg: APP and Intracellular Aβ Balance Critical

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Recent studies have demonstrated that wild-type APP can protect against p53 mediated apoptosis, whereas FAD mutant APP (FADAPP) cannot. N3 rat neuroblastoma cells which are deficient in APP were transfected with wtAPP or FADAPP and the

Society for Neuroscience Annual Meeting: α1-Antichymotrypsin

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Yamin (122.9) presented evidence that the zinc metalloproteinase EC 3.4.24.15 (E24.15) plays a role in neuronal mediated degradation of Aβ. In fact transfection of neuroblastoma cells with antisense E24.15 allows the accumulation of Aβ

Society for Neuroscience Annual Meeting: Making the Right Mouse Model?

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Several groups have reported a lack of phenotype in α-synuclein (α-S) transgenic mice, but it appears Lennart Mucke (122.10) has got it right. Mucke reported that inclusion bodies were obvious in PDGF promoter-driven α-S Tg mice as ear

Society for Neuroscience Annual Meeting: Enzyme Mediates Aβ Degradation

CONFERENCE COVERAGE 1999-10-24 Conference Coverage Previous studies on the purification and characterization of the predominant extracellular Aβ degrading activity in the murine BV-2 microglial cell line demonstrated that insulin-degrading enzyme (IDE) or a novel protease indistinguish

Soc for Neuroscience Ann Mtg: Novel Assay for in Vivo Catabolism of Aβ

CONFERENCE COVERAGE 1999-10-24 Conference Coverage The N- and C-terminals of synthetic Aβ1-42 were differentially labeled with 3H and 14C and then used as a probe to measure degradation by injection into rat hippocampus. Effects of various protease inhibitors and two dimensional HPLC a

Soc for Neuroscience Annual Meeting: Novel Receptor Interaction for Aβ

CONFERENCE COVERAGE 1999-10-24 Conference Coverage That β-amyloid plays a central role in the pathogenesis of Alzheimer's disease is doubted by few investigators. However, pinning down the exact contribution amyloid makes has been remarkably difficult to accomplish. Novel hypothes