All Comments by Ilya Bezprozvanny

  1. Presenilin-1 knockin mice reveal loss-of-function mechanism for familial Alzheimer's disease.
  2. ER-mitochondria associations are regulated by the VAPB-PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43.
  3. Cytotoxicity of intracellular aβ42 amyloid oligomers involves Ca2+ release from the endoplasmic reticulum by stimulated production of inositol trisphosphate.
  4. First Crystal Structure of a Presenilin
  5. Early presynaptic and postsynaptic calcium signaling abnormalities mask underlying synaptic depression in presymptomatic Alzheimer's disease mice.
  6. Single-channel Ca(2+) imaging implicates Aβ1-42 amyloid pores in Alzheimer's disease pathology.
  7. A synaptic vesicle-associated Ca2+ channel promotes endocytosis and couples exocytosis to endocytosis.
  8. Presenilins, Ryanodine Receptors—Conspirators in Neurotransmission?
  9. Perpetrator and Savior—Presenilins Cut Both Ways
  10. NAADP mobilizes calcium from acidic organelles through two-pore channels.
  11. A polymorphism in CALHM1 influences Ca2+ homeostasis, Abeta levels, and Alzheimer's disease risk.
  12. Mechanism of Ca2+ disruption in Alzheimer's disease by presenilin regulation of InsP3 receptor channel gating.
  13. Presenilin Loss of Function—Plan B for AD?
  14. Presenilins Open Escape Hatch for ER Calcium
  15. Calcium dysregulation in Alzheimer's disease: recent advances gained from genetically modified animals.