An APP-Presenilin Connection
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?...
ALL NEWS
5889 RESULTS
Sort By:
- Most Recent
- Most Commented
What FTDP-17 Mutations Do
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...
Hungarian Conference on Alzheimer's Disease and Related Disorders 1998
News Coverage of the 4th Hungarian Conference on AD: Hungarian Conference on Alzheimer's Disease and Related Disorders 1998
Genome-wide Gene Screening Goes Live
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...
News Coverage of the 4th Hungarian Conference on AD:
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...
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...
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: 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: 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: 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: 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: 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 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: 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)...
Current Filters
No filters selected