All Comments by Jürgen Götz

  1. Activity-dependent tau protein translocation to excitatory synapse is disrupted by exposure to amyloid-beta oligomers.
  2. Sustained peripheral depletion of amyloid-β with a novel form of neprilysin does not affect central levels of amyloid-β.
  3. Soluble pathological tau in the entorhinal cortex leads to presynaptic deficits in an early Alzheimer's disease model.
  4. Two novel tau antibodies targeting the 396/404 region are primarily taken up by neurons and reduce tau pathology.
  5. Amyloid-β oligomers induce synaptic damage via Tau-dependent microtubule severing by TTLL6 and spastin.
  6. Proteomics Point to RNA Splicing Defects in Alzheimer’s
  7. Pooled GWAS Reveals New Alzheimer’s Genes and Pathways
  8. The hallmarks of aging.
  9. Formaldehyde induces hyperphosphorylation and polymerization of Tau protein both in vitro and in vivo.
  10. Tau loss attenuates neuronal network hyperexcitability in mouse and Drosophila genetic models of epilepsy.
  11. Interaction of Endogenous Tau Protein with Synaptic Proteins Is Regulated by N-Methyl-D-aspartate Receptor-dependent Tau Phosphorylation.
  12. Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons.
  13. Calpain Inhibitor A-705253 Mitigates Alzheimer's Disease-Like Pathology and Cognitive Decline in Aged 3xTgAD Mice.
  14. Neuronal mRNAs travel singly into dendrites.
  15. Pinning Down Role for Tau Proline Isomers in Alzheimer’s