All Comments by Takaomi Saido

  1. Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.
  2. Conjugal Alzheimer disease: risk in children when both parents have Alzheimer disease.
  3. GSK3 alpha and GSK3 beta are necessary for axon formation.
  4. N-terminal cleavage of GSK-3 by calpain: a new form of GSK-3 regulation.
  5. A high-density whole-genome association study reveals that APOE is the major susceptibility gene for sporadic late-onset Alzheimer's disease.
  6. Abeta40 protects non-toxic Abeta42 monomer from aggregation.
  7. Effects of hypoxia and oxidative stress on expression of neprilysin in human neuroblastoma cells and rat cortical neurones and astrocytes.
  8. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model.
  9. GSK3beta activity modifies the localization and function of presenilin 1.
  10. The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.
  11. Implications of co-morbidity for etiology and treatment of neurodegenerative diseases with multifunctional neuroprotective-neurorescue drugs; ladostigil.
  12. Anatomical integration of newly generated dentate granule neurons following traumatic brain injury in adult rats and its association to cognitive recovery.
  13. The proline-rich domain and the microtubule binding domain of protein tau acting as RNA binding domains.
  14. The DYRK1A gene, encoded in chromosome 21 Down syndrome critical region, bridges between beta-amyloid production and tau phosphorylation in Alzheimer disease.
  15. On the seeding and oligomerization of pGlu-amyloid peptides (in vitro).