All Comments by Takaomi Saido

  1. Adaptive responses to alloxan-induced mild oxidative stress ameliorate certain tauopathy phenotypes.
  2. Pseudohyperphosphorylation has differential effects on polymerization and function of tau isoforms.
  3. Resolving Controversies on the Path to AD Therapeutics
  4. Resolving controversies on the path to Alzheimer's therapeutics.
  5. Selective hippocampal neurodegeneration in transgenic mice expressing small amounts of truncated Aβ is induced by pyroglutamate-Aβ formation.
  6. Activation of matrix metalloproteinases following anti-Aβ immunotherapy; implications for microhemorrhage occurrence.
  7. Opposing synaptic regulation of amyloid-β metabolism by NMDA receptors in vivo.
  8. Presymptomatic apolipoprotein E genotyping for Alzheimer's disease risk assessment and prevention.
  9. Time course of glucose metabolism in relation to cognitive performance and postmortem neuropathology in Met146Val PSEN1 mutation carriers.
  10. Power and pitfalls of the genome-wide association study approach to identify genes for Alzheimer's disease.
  11. Factors responsible for neurofibrillary tangles and neuronal cell losses in tauopathy.
  12. Dissociation of apolipoprotein E oligomers to monomer is required for high-affinity binding to phospholipid vesicles.
  13. Combinatorial Tau pseudophosphorylation: markedly different regulatory effects on microtubule assembly and dynamic instability than the sum of the individual parts.
  14. Two distinct amyloid beta-protein (Abeta) assembly pathways leading to oligomers and fibrils identified by combined fluorescence correlation spectroscopy, morphology, and toxicity analyses.
  15. What was lost in translation in the DHA trial is whom you should intend to treat.