All Comments by Takaomi Saido

  1. GSK3beta activity modifies the localization and function of presenilin 1.
  2. The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.
  3. Implications of co-morbidity for etiology and treatment of neurodegenerative diseases with multifunctional neuroprotective-neurorescue drugs; ladostigil.
  4. Anatomical integration of newly generated dentate granule neurons following traumatic brain injury in adult rats and its association to cognitive recovery.
  5. The proline-rich domain and the microtubule binding domain of protein tau acting as RNA binding domains.
  6. The DYRK1A gene, encoded in chromosome 21 Down syndrome critical region, bridges between beta-amyloid production and tau phosphorylation in Alzheimer disease.
  7. On the seeding and oligomerization of pGlu-amyloid peptides (in vitro).
  8. Enhanced amyloidogenic metabolism of the amyloid beta-protein precursor in the X11L-deficient mouse brain.
  9. Unraveling in vivo functions of amyloid precursor protein: insights from knockout and knockdown studies.
  10. A genomic screen for modifiers of tauopathy identifies puromycin-sensitive aminopeptidase as an inhibitor of tau-induced neurodegeneration.
  11. Accumulation of amyloid precursor protein in the mitochondrial import channels of human Alzheimer's disease brain is associated with mitochondrial dysfunction.
  12. Studies to investigate the in vivo therapeutic window of the gamma-secretase inhibitor N2-[(2S)-2-(3,5-difluorophenyl)-2-hydroxyethanoyl]-N1-[(7S)-5-methyl-6-oxo-6,7-dihydro-5H-dibenzo[b,d]azepin-7-yl]-L-alaninamide (LY411,575) in the CRND8 mouse.
  13. Functional modulation of parkin through physical interaction with SUMO-1.
  14. Frontotemporal dementia-like phenotypes associated with presenilin-1 mutations.
  15. Deletion of the ubiquitin ligase CHIP leads to the accumulation, but not the aggregation, of both endogenous phospho- and caspase-3-cleaved tau species.