339113 RESULTS
INTERVIEWS 1999-01-26 Interviews ARF: What’s the primary hypothesis that guides your lab group? RN: We’ve said for many years that we think that the carboxy terminal fragment of APP, that we call C100, which would result from cleavage at the N-terminus of the A-beta sequence,
INTERVIEWS 1999-01-18 Interviews ARF: What is the primary hypothesis that guides your laboratory? PC: The primary hypothesis that guides my laboratory shifts from time to time as we and other people get more data; but the primary hypothesis in the lab now is that a cell in AD
INTERVIEWS 1999-01-08 Interviews ARF: What is the primary hypothesis that drives your lab group? DS: The primary hypothesis is that a chronic imbalance in the production versus the clearance of Aβ leading to a gradual rise in its steady state levels in brain tissue is the caus
INTERVIEWS 1998-12-22 Interviews HP: One of the few things about Alzheimer's disease on which everyone basically agrees is that it starts 20 or 30 years before the first symptoms. That means, when we look in an AD brain, we are looking at the very last stages of the proce
INTERVIEWS 1998-12-15 Interviews ARF: I appreciate your taking the time to talk to me. JT: I am pleased to do this, since, although my major focus as a biomedical researcher is to try to unravel the causes and mechanisms of neurodegenerative disorders such as Alzheimer's
CONFERENCE COVERAGE SERIES American Society for Cell Biology 38th Annual Meeting: Tau Protein in Neurodegenerative Diseases American Society for Cell Biology 38th Annual Meeting: More About Tau American Society for Cell Biology 38th Annual Meeting: Novel Protein Binds to APP and Mi
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Maas et al. (Abstract 2285) studied how phosphorylation of two different regions in tau proteins affects binding of tau protein to the plasma-membrane (PM). The two major phosphorylation sites studied were those located just upstream o
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Tau protein in Neurodegenerative Diseases A special interest subgroup meeting on 'Tau protein in Neurodegenerative Diseases' was organized by Gloria Lee, University of Iowa. This was a timely and stimulating meeting, that was
CONFERENCE COVERAGE 1998-12-12 Conference Coverage A special interest subgroup meeting on "Tau protein in Neurodegenerative Diseases" was organized by Gloria Lee, University of Iowa. This was a timely and stimulating meeting that was energized in large part by the recent disc
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Zheng et al. (Abstract 516) described the characterization of PAT1, a novel protein that binds to an 11-residue segment of the amyloid precursor protein (APP) in yeast 2-hybrid assays. PAT1 also bind to microtubules (MT). When coexpres
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Holtzman et al. (Abstract 612) reported that 95 percent of immunoreactive β-amyloid in human cerebral spinal fluid is bound to the ER chaperone Erp57. Anti-Erp57 and anti-Aβ antibodies were found to react with an approximately 62 kDα b
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Harada et al. (Abstract 902) have now disrupted the MAP2 gene in mouse. Like tau and MAP1B knockout mice, MAP-2 knockout mice are fertile and have apparently normal brain cytoarchitecture. Interestingly, double tau and MAP1B knockout m
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Chan et al. (Abstract 1421) used immunoblot analysis to quantitatively demonstrate that the polypeptides corresponding to AMPA (GluR2 and 3) and NMDA subfamilies of the glutamate receptors are decreased in AD brain lysates compared to
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Mervyn Monteiro (the author of this report) and colleagues described the identification and characterization of two different proteins that interact with presenilins in the yeast-2 hybrid interaction trap (Y2H). Stabler et al. (Abstrac
CONFERENCE COVERAGE 1998-12-12 Conference Coverage Monteiro and Janicki et al. (Abstract 1057) showed by BrdU labeling of HeLa cells that overexpression of both PS1 and PS2 arrest cells in the G1 phase of the cell cycle. This arrest presumably precedes apoptosis of the cells which this
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