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...
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...
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 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...
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...
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...
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...
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...
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...
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...
The idea of treating developmental and neurodegenerative disorders by growing new brain cells has taken a major step forward, according to results of two studies...
Can transgenic mice serve as a truly useful model for studying Alzheimer's disease? Studies of mice expressing an APP gene mutation that causes a form of familial AD have reported no neuronal loss...
Since the discovery that mutations in the gene for PS1 cause familial Alzheimer disease, there has been keen interest in investigating the mechanism by which PS1 mutations cause disease...