All Comments by Nikolaos K. Robakis

  1. Evidence for lymphatic Aβ clearance in Alzheimer's transgenic mice.
  2. Coordination between proteasome impairment and caspase activation leading to TAU pathology: neuroprotection by cAMP.
  3. Testing the right target and right drug at the right stage.
  4. Intraneuronal APP, not free Aβ peptides in 3xTg-AD mice: implications for tau versus Aβ-mediated Alzheimer neurodegeneration.
  5. Reversing EphB2 depletion rescues cognitive functions in Alzheimer model.
  6. Higher incidence of mild cognitive impairment in familial hypercholesterolemia.
  7. γ-Secretase Drives Spine Formation Via Novel Substrate
  8. Cerebral amyloid angiopathy and parenchymal amyloid deposition in transgenic mice expressing the Danish mutant form of human BRI2.
  9. Presenilin Loss of Function—Plan B for AD?
  10. Protease or Not?—More to Presenilin Toxicity than Meets the (Fly's) Eye
  11. Deletion of presenilin 1 hydrophilic loop sequence leads to impaired gamma-secretase activity and exacerbated amyloid pathology.
  12. Gain or Loss of Function—Time to Shake up Assumptions on γ-Secretase in Alzheimer Disease?
  13. Dangerous Liaisons—Tau and Aβ, Together at Last?
  14. Brain-derived neurotrophic factor induces a rapid dephosphorylation of tau protein through a PI-3 Kinase signalling mechanism.
  15. Specific inhibition of CBP/beta-catenin interaction rescues defects in neuronal differentiation caused by a presenilin-1 mutation.