All Comments by Edward Koo
- Mutant ubiquitin found in neurodegenerative disorders is a ubiquitin fusion degradation substrate that blocks proteasomal degradation.
- Postischemic hyperthermia induces Alzheimer-like pathology in the rat brain.
- Alpha-synuclein-immunoreactive deposits in human and animal prion diseases.
- Peeling plaque. Researchers remain optimistic about a vaccine against Alzheimer's.
- FAD mutant PS-1 gene-targeted mice: increased A beta 42 and A beta deposition without APP overproduction.
- Beta-secretase processing in the trans-Golgi network preferentially generates truncated amyloid species that accumulate in Alzheimer's disease brain.
- Receptor-dependent cell stress and amyloid accumulation in systemic amyloidosis.
- A novel epsilon-cleavage within the transmembrane domain of the Alzheimer amyloid precursor protein demonstrates homology with Notch processing.
- Copernicus revisited: amyloid beta in Alzheimer's disease.
- A gene trap insertion reveals that amyloid precursor protein expression is a very early event in murine embryogenesis.
- Gamma-secretase-like cleavages of Notch and beta APP are mutually exclusive in human cells.
- Reduced effectiveness of Abeta1-42 immunization in APP transgenic mice with significant amyloid deposition.
- Nonsteroidal antiinflammatory drugs and the risk of Alzheimer's disease.
- Treatment with controlled-release lovastatin decreases serum concentrations of human beta-amyloid (A beta) peptide.
- APP transgenic mice Tg2576 accumulate Abeta peptides that are distinct from the chemically modified and insoluble peptides deposited in Alzheimer's disease senile plaques.