All Comments by Nikolaos K. Robakis
- Brain-derived neurotrophic factor induces a rapid dephosphorylation of tau protein through a PI-3 Kinase signalling mechanism.
- Specific inhibition of CBP/beta-catenin interaction rescues defects in neuronal differentiation caused by a presenilin-1 mutation.
- Presenilins Work Overtime to Control Akt, Tau, and Aβ—n-3 Fatty Acids Aid and Abet
- Familial Alzheimer's disease mutations inhibit gamma-secretase-mediated liberation of beta-amyloid precursor protein carboxy-terminal fragment.
- Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice.
- Neuronal dysfunction in a polyglutamine disease model occurs in the absence of ubiquitin-proteasome system impairment and inversely correlates with the degree of nuclear inclusion formation.
- Presenilin 2 familial Alzheimer's disease mutations result in partial loss of function and dramatic changes in Abeta 42/40 ratios.
- Poles Apart—The Tau Kinase GSK3β Separates Axons and Dendrites
- Hemorrhage is uncommon in new Alzheimer family with Flemish amyloid precursor protein mutation.
- MARKing tau for tangles and toxicity.
- Got RIP? Presenilin-dependent intramembrane proteolysis in growth factor receptor signaling.
- Interference of human and Drosophila APP and APP-like proteins with PNS development in Drosophila.
- APP processing is regulated by cytoplasmic phosphorylation.
- Ordered-subsets linkage analysis detects novel Alzheimer disease loci on chromosomes 2q34 and 15q22.
- APP-BP1 mediates APP-induced apoptosis and DNA synthesis and is increased in Alzheimer's disease brain.