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Three abstracts presented during this session, as well as those by Vincent et al. (Abstract 594) and Arendt et al. (Abstract 595), indicate that cell cycle and mitotic mechanisms may be a key factor in the understanding of tau phosphorylation...
If you came to Amsterdam hoping to hear a lot of new data on Aβ peptide inhibitors, you might have learned more by window shopping in the red-light district...
Over a decade ago, John Blass and his colleagues proposed that AD was caused by compromised metabolism. Today, this theory has gained support from a convergence of numerous...
The focus of this symposium was the biology and diagnostic value of a recently discovered protein, termed AD7c-neuronal thread protein (NTP), in Alzheimer's disease...
Yamaguchi (Abstract 1245) presented his theory that very diffuse plaques within nondemented individuals are cleared by astrocytic phagocytosis. He showed many examples of very diffuse Aβ-positive staining...
A new epidemic of "mad tau disease" swept Amsterdam at the workshop on Hereditary Fronto-Temporal Dementia and Pick's disease. Fronto-temporal dementia and Parkinsonism linked to chromosome 17...
While a number of drug companies have been pumping big bucks into creating novel molecules capable of inhibiting formation of Aβ fibrils, along comes Alan Snow and his colleagues...
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...
Fred van Leeuwen and his research group presented new data regarding their molecular misreading hypothesis for sporadic AD (Abstract 107.7)...
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...
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...
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...
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...
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...
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...
