6234 RESULTS
INTERVIEWS 1998-12-10 Interviews During his medical school training in neurology at Harvard, Bruce Yankner was drawn into the Alzheimer field when he found that an APP gene construct (C100) was toxic to neurons. "Alzheimer's disease was one of few neurodegenerative d
RESEARCH NEWS 1998-12-08 Research News Mutations in the β-amyloid precursor protein (APP), presenilin-1 and presenilin-2 cause inherited forms of Alzheimer's disease, but how do these protein interact, normally and in the disease process? In 1996, researchers Nazneen Dewji a
RESEARCH NEWS 1998-12-04 Research News A new study elucidates the molecular mechanisms that may explain how mutations of the tau gene give rise to frontotemporal dementia and parkinsonism (FTDP-17), an inherited disorder that is similar to Alzheimer's disease. In this week&#
RESEARCH NEWS 1998-12-01 Research News (From Nature Biotechnology Press Release.) Current estimates predict that genome sequencing efforts may reveal between 3,000 and 10,000 new targets for drugs. In the December issue of Nature Biotechnology, Paul Negulescu and colleagues descr
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
