All Comments by Virgil Muresan

  1. Reply: the early pathological process in sporadic Alzheimer's disease.
  2. Loss of c-Jun N-terminal kinase-interacting protein-1 does not affect axonal transport of the amyloid precursor protein or Aβ production.
  3. Neural Activity Tips Endosomal Balance, Hastens Amyloid Pathology
  4. Proteomics Point to RNA Splicing Defects in Alzheimer’s
  5. Modeling Alzheimer's disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness.
  6. JNK3 perpetuates metabolic stress induced by Aβ peptides.
  7. Coming Into Vogue? Retromer in APP Processing, AD Pathogenesis
  8. Axonal transport deficits and degeneration can evolve independently in mouse models of amyotrophic lateral sclerosis.
  9. Impaired β-amyloid secretion in Alzheimer's disease pathogenesis.
  10. APP is phosphorylated by TrkA and regulates NGF/TrkA signaling.
  11. LRAD3, a novel low-density lipoprotein receptor family member that modulates amyloid precursor protein trafficking.
  12. Intraneuronal APP, not free Aβ peptides in 3xTg-AD mice: implications for tau versus Aβ-mediated Alzheimer neurodegeneration.
  13. Neuronal activity regulates the regional vulnerability to amyloid-β deposition.
  14. Alzheimer's pathogenesis: is there neuron-to-neuron propagation?
  15. Herpes simplex virus dances with amyloid precursor protein while exiting the cell.