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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...
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...
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...
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...
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...
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...
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...
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...
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...
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...
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...
It is likely that a process very reminiscent of that suggested for Aβ formation—fibrillar protein deposition—is to blame for the rare, inherited disorder Familial British Dementia (FBD)...
According to a report in tomorrow's Science, researchers have uncovered a strong candidate for β-secretase, the mystery enzyme that cleaves APP and allows Aβ to be formed in subsequent cleavages...
From today's Journal of Neuroscience comes evidence that intermediate Aβ species could be damaging neurons. Dean Hartley, Dennis Selkoe, and their colleagues report that so-called "protofibrillar" Aβ...
Further evidence that apoE is needed for deposition of the fibrillar form of Aβ in plaques was presented today at the American Neurological Association's annual meeting in Seattle today...
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