CONFERENCE COVERAGE SERIES
Society for Neuroscience Annual Meeting 1998
Los Angeles, California, U.S.A.
07 – 12 November 1998
1998 Society for Neuroscience Meeting: α2-Macroglobulin
AD is now widely considered to be a multifactorial disease with only a few dominant genetic mutations that can be considered as directly causing the disease, i.e., APP and the presenilins...
1998 Society of Neuroscience Meeting: AD Plaques Associated with Curvier Dendrites
Are both Aβ and the intracellular hyperphosphorylation of tau necessary for the induction of morphological alterations in dendrites in AD?...
1998 Society for Neuroscience Meeting: Aβ vs. APP Effects in Transgenics
Hopefully, transgenic AD models will be more useful than just demonstrating that the overexpression of mutant human APP can lead to the deposition of Aβ plaques...
1998 Society for Neuroscience Meeting: Frameshift Mutations Precede Tangles, Plaques in DS
Fred van Leeuwen and his research group presented new data regarding their molecular misreading hypothesis for sporadic AD (Abstract 107.7)...
1998 Society for Neuroscience Meeting: Complement Cascade Activation by Neurofibrillary Tangles
The complement cascade is a complex inflammatory process that can mediate diverse functions, from targeting cells and cellular components for phagocytosis to membrane attack complex-mediated cell death...
1998 Society for Neuroscience Meeting: Untangling Tau Phosphorylation
Aβ peptide has dominated center stage in AD research, but the discovery last year of a tau mutation that causes a familial non-AD dementia has reawakened broader interest in tau...
1998 Society for Neuroscience Meeting: Alois Award Winners
The organizers of this year's special interest social on Alzheimer's disease decided to stage an awards ceremony to salute scientists who had distinguished themselves in various categories not ordinarily recognized...
1998 Society for Neuroscience Meeting: Amyloid Plus Astrocytes Thwarts Axon Regeneration
The regulation of neuronal plasticity and regeneration in the CNS is an aspect of Alzheimer’s disease that often has to compete with the big stars, such as amyloid or presenilin, for attention...
1998 Society for Neuroscience Meeting: Enhancement of Pathology in PS1/APP Tg Mice
There have been several reports over the years that the AD brain exhibits deficits in energy metabolism. In 1994, Yankner's group reported that sodium azide treatment increased...
1998 Society for Neuroscience Meeting: Inflammatory Mechanisms in Transgenic Models of AD
Since the development of transgenic models of β-amyloid plaque formation, considerable debate has developed over the apparent paucity of neuronal cell loss found in the majority of these models...
1998 Society for Neuroscience Meeting: Lesion Lops Aβ Deposition
The Athena Neuroscience PDAPP transgenic mice develop heavy Aβ deposits, particularly in the outer molecular layer (OML) of the dentate gyrus, a region that receives nerve projections from the entorhinal cortex...
1998 Society for Neuroscience Meeting: ApoE Knockouts Unaffected in APP Expression and Processing
The critical role of ApoE in β-amyloid deposition was demonstrated last year by Eli Lilly scientists, who crossbred APP/PS1 transgenics with an ApoE knockout and found...