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CONFERENCE COVERAGE 1998-12-01 Conference Coverage Introduction: This annual meeting had significant international participation with 14 different countries being represented and, whilst comprehensive, the meeting focused on the cholinergic system, therapeutics and new findings. The op
CONFERENCE COVERAGE 1998-11-12 Conference Coverage 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 that these mice do not develop thioflavin S-positive deposits of fi
CONFERENCE COVERAGE 1998-11-11 Conference Coverage 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. Yet, it is clear that understanding the f
CONFERENCE COVERAGE 1998-11-11 Conference Coverage 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. One hypothesis for why there is an overa
CONFERENCE COVERAGE 1998-11-11 Conference Coverage 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 the processing of APP to potentially amyloidogenic fr
CONFERENCE COVERAGE 1998-11-11 Conference Coverage 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. Theorizing that neurona
CONFERENCE COVERAGE 1998-11-11 Conference Coverage 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 by the com
CONFERENCE COVERAGE 1998-11-10 Conference Coverage 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. In this context, there are 20 or
CONFERENCE COVERAGE 1998-11-10 Conference Coverage 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. In Alzheimer’s disease, tau aggregates into pathological
CONFERENCE COVERAGE 1998-11-08 Conference Coverage Are both Aβ and the intracellular hyperphosphorylation of tau necessary for the induction of morphological alterations in dendrites in AD? What effect might abnormally shaped dendrites have on synaptic transmission? Using triple labeli
CONFERENCE COVERAGE 1998-11-08 Conference Coverage Fred van Leeuwen and his research group presented new data regarding their molecular misreading hypothesis for sporadic AD (Abstract 107.7). The molecular misreading hypothesis suggests that the inaccurate conversion of genomic informa
CONFERENCE COVERAGE 1998-11-08 Conference Coverage 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. Several groups are now asking, what are the functional consequences of th
CONFERENCE COVERAGE 1998-11-07 Conference Coverage Presented by Rudy Tanzi. 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. The majority of genet
RESEARCH NEWS 1998-11-05 Research News It is known that aspirin and sodium salicylate suppress inflammation by inhibiting cyclooxygenase, an enzyme that triggers production of prostaglandin. It has been suspected that these compounds also exert their anti-inflammatory effects thr
RESEARCH NEWS 1998-10-30 Research News It has long been a dogma of neuroscience that the human brain is born with all the neurons it will ever have, and that those neurons must endure for a lifetime. But evidence has been accumulating that this dogma may not strictly be true. Neu
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