All Comments by

  1. Hiroshi Mori on Neurogenic phenotypes and altered Notch processing in Drosophila Presenilin mutants.
  2. Paul Coleman on The regulation of phosphorylation of tau in SY5Y neuroblastoma cells: the role of protein phosphatases.
  3. Nikolaos K. Robakis on Apolipoprotein E isoform-specific reduction of extracellular amyloid in neuronal cultures.
  4. Hiroshi Mori on Phosphorylation of presenilin-2 regulates its cleavage by caspases and retards progression of apoptosis.
  5. John Olney on beta-Amyloid peptide-induced morphological changes coincide with increased K+ and Cl- channel activity in rat cortical astrocytes.
  6. Paul Coleman on Environmental enrichment inhibits spontaneous apoptosis, prevents seizures and is neuroprotective.
  7. Benjamin Wolozin on Dementia with Lewy bodies treated with rivastigmine: effects on cognition, neuropsychiatric symptoms, and sleep.
  8. Hiroshi Mori on Altered calcium homeostasis and mitochondrial dysfunction in cortical synaptic compartments of presenilin-1 mutant mice.
  9. Paul Coleman on Free D- and L-amino acids in ventricular cerebrospinal fluid from Alzheimer and normal subjects.
  10. Hiroshi Mori on Cerebrovascular accumulation and increased blood-brain barrier permeability to circulating Alzheimer's amyloid beta peptide in aged squirrel monkey with cerebral amyloid angiopathy.
  11. Carl Cotman on Beta-secretase processing of the beta-amyloid precursor protein in transgenic mice is efficient in neurons but inefficient in astrocytes.
  12. Edward Koo on Calpain-mediated degradation of p35 to p25 in postmortem human and rat brains.
  13. Carl Cotman on Frontal lobe degeneration of non-Alzheimer type. Structural characteristics, diagnostic criteria and relation to other frontotemporal dementias.
  14. Hiroshi Mori on Endoplasmic reticulum and trans-Golgi network generate distinct populations of Alzheimer beta-amyloid peptides.
  15. Carl Cotman on In situ labeling of dying cortical neurons in normal aging and in Alzheimer's disease: correlations with senile plaques and disease progression.