All Comments by Gunnar Gouras

  1. Differential Release of β-Amyloid from Dendrite- Versus Axon-Targeted APP.
  2. Activity-Induced Convergence of APP and BACE-1 in Acidic Microdomains via an Endocytosis-Dependent Pathway.
  3. Spike bursts increase amyloid-β 40/42 ratio by inducing a presenilin-1 conformational change.
  4. Like Star Born of Supernova, Plaque Born of Exploded Neuron?
  5. The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus.
  6. Barreling Down Amyloid Plaque Distribution
  7. Amyloid precursor protein (APP) traffics from the cell surface via endosomes for amyloid β (Aβ) production in the trans-Golgi network.
  8. Epilepsy Drug Calms the Hippocampus, Aids Memory
  9. Modification of γ-secretase by nitrosative stress links neuronal ageing to sporadic Alzheimer's disease.
  10. FBL2 regulates amyloid precursor protein (APP) metabolism by promoting ubiquitination-dependent APP degradation and inhibition of APP endocytosis.
  11. Intracellular Aβ Causes Neurodegeneration in Mice
  12. Induced Neurons From AD Patients Hint at Disease Mechanisms
  13. Testing the right target and right drug at the right stage.
  14. Dynamic analysis of amyloid β-protein in behaving mice reveals opposing changes in ISF versus parenchymal Aβ during age-related plaque formation.
  15. Intraneuronal APP, not free Aβ peptides in 3xTg-AD mice: implications for tau versus Aβ-mediated Alzheimer neurodegeneration.