All Comments by Nikolaos K. Robakis

  1. Presenilins Work Overtime to Control Akt, Tau, and Aβ—n-3 Fatty Acids Aid and Abet
  2. Familial Alzheimer's disease mutations inhibit gamma-secretase-mediated liberation of beta-amyloid precursor protein carboxy-terminal fragment.
  3. Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice.
  4. 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.
  5. Presenilin 2 familial Alzheimer's disease mutations result in partial loss of function and dramatic changes in Abeta 42/40 ratios.
  6. Poles Apart—The Tau Kinase GSK3β Separates Axons and Dendrites
  7. Hemorrhage is uncommon in new Alzheimer family with Flemish amyloid precursor protein mutation.
  8. MARKing tau for tangles and toxicity.
  9. Got RIP? Presenilin-dependent intramembrane proteolysis in growth factor receptor signaling.
  10. Interference of human and Drosophila APP and APP-like proteins with PNS development in Drosophila.
  11. APP processing is regulated by cytoplasmic phosphorylation.
  12. Ordered-subsets linkage analysis detects novel Alzheimer disease loci on chromosomes 2q34 and 15q22.
  13. APP-BP1 mediates APP-induced apoptosis and DNA synthesis and is increased in Alzheimer's disease brain.
  14. Society for Neuroscience Annual Meeting: Presenilins: An Overview
  15. Striation is the characteristic neuritic abnormality in Alzheimer disease.