All Comments by Andre Delacourte

  1. Presenilin Loss of Function—Plan B for AD?
  2. Modulation of synaptic plasticity and Tau phosphorylation by wild-type and mutant presenilin1.
  3. The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.
  4. Collective Thought at Its Best: Let’s Contemplate the Centennial
  5. BACE1 inhibition reduces endogenous Abeta and alters APP processing in wild-type mice.
  6. Neuroprotective effects of (-)-epigallocatechin-3-gallate in a transgenic mouse model of amyotrophic lateral sclerosis.
  7. An inhibitor of tau hyperphosphorylation prevents severe motor impairments in tau transgenic mice.
  8. An immunohistochemical study of cases of sporadic and inherited frontotemporal lobar degeneration using 3R- and 4R-specific tau monoclonal antibodies.
  9. Mechanisms of action of green tea catechins, with a focus on ischemia-induced neurodegeneration.
  10. Reduction of Abeta levels in the Sprague Dawley rat after oral administration of the functional gamma-secretase inhibitor, DAPT: a novel non-transgenic model for Abeta production inhibitors.
  11. Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice.
  12. APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy.
  13. Suppression of cyclin-dependent kinase 5 activation by amyloid precursor protein: a novel excitoprotective mechanism involving modulation of tau phosphorylation.
  14. Beta-site APP cleaving enzyme 1 (BACE1) is increased in remaining neurons in Alzheimer's disease brains.
  15. Progressive neuronal loss and behavioral impairments of transgenic C57BL/6 inbred mice expressing the carboxy terminus of amyloid precursor protein.