346623 RESULTS
CONFERENCE COVERAGE 1998-07-22 Conference Coverage Yamaguchi (Abstract 1245) presented his theory that very diffuse plaques within nondemented individuals are cleared by astrocytic phagocytosis. He showed many examples of very diffuse Aβ-positive staining within the brains of 40-50 yea
CONFERENCE COVERAGE 1998-07-22 Conference Coverage A new epidemic of "mad tau disease" swept Amsterdam at the workshop on Hereditary Fronto-Temporal Dementia and Pick's disease. Fronto-temporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) has been linked t
CONFERENCE COVERAGE 1998-07-22 Conference Coverage While a number of drug companies have been pumping big bucks into creating novel molecules capable of inhibiting formation of Aβ fibrils, along comes Alan Snow and his colleagues at the University of Washington and his Seattle-based co
CONFERENCE COVERAGE 1998-07-21 Conference Coverage If you came to Amsterdam hoping to hear a lot of new data on Aβ peptide inhibitors, you might have learned more by window shopping in the red-light district. This doesn't mean that the session was without merit. Barbara Cordell (A
CONFERENCE COVERAGE 1998-07-21 Conference Coverage Over a decade ago, John Blass and his colleagues proposed that AD was caused by compromised metabolism. Today, this theory has gained support from a convergence of numerous therapeutic, pathological and biochemical studies pointing to
CONFERENCE COVERAGE 1998-07-21 Conference Coverage 21 July 1998. The focus of this symposium was the biology and diagnostic value of a recently discovered protein, termed AD7c-neuronal thread protein (NTP), in Alzheimer's disease (AD). Dr. Suzanne de la Monte presented the discove
CONFERENCE COVERAGE 1998-07-20 Conference Coverage The "great amyloid debate" appeared to resolve at least one issue in the rather contentious arena of defining the critical neuropathological events in AD. Amyloid per se, i.e., "extracellular, fibrillar, congophilic depo
CONFERENCE COVERAGE 1998-07-20 Conference Coverage Aβ's fibril-formation processes were revealed in a tour de force of atomic force microscopy by Harper (Abstract 909). The initial species to be detected are four nm globular assemblies which range in size from 1.4 to 14 nm. He ind
CONFERENCE COVERAGE 1998-07-20 Conference Coverage Three abstracts presented during this session, as well as those by Vincent et al. (Abstract 594) and Arendt et al. (Abstract 595), indicate that cell cycle and mitotic mechanisms may be a key factor in the understanding of tau phosphor
CONFERENCE COVERAGE 1998-07-19 Conference Coverage This roundtable session, supported by a grant from SmithKline Beecham and cochaired by G. Wilcock (Bristol, UK) and R. Kumar (Essex, UK), sought to provide a glimpse of future directions for the development of new therapeutic agents fo
CONFERENCE COVERAGE 1998-07-19 Conference Coverage B. Mahley (Abstract 303) reported new data on transgenic mice that could help elucidate the role of ApoE isoforms in neurodegeneration. He began his lecture with an overview of the structure and function of apolipoprotein E (ApoE), a l
CONFERENCE COVERAGE 1998-07-19 Conference Coverage Alonso et al. (Abstract 590) reviewed the role of tau proteins in tubulin polymerization. There are six tau isoforms in the human brain. Three have three microtubule-binding domains (3R) and the three others have four microtubule-bindi
CONFERENCE COVERAGE 1998-07-18 Conference Coverage Perhaps one of the most striking features of the conference this year, reflecting the state of research on AD in general, is the continued absence of a clear consensus on what is the most relevant neuropathological change in AD. The fi
CONFERENCE COVERAGE 1998-07-18 Conference Coverage This session was disappointing, offering nothing really new. What new data were presented appear to be very controversial. Farrer et al. (Abstract 280) tried to confirm the linkage described by Duke University, North Carolina. They des
CONFERENCE COVERAGE 1998-07-18 Conference Coverage Soto (Abstract 295) presented data documenting the ability of their 11 and 5 amino-acid inhibitors to inhibit initial Aβ peptide aggregation and its ability to dissociate already formed Aβ fibrils in vitro. In addition to the assays me
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