All Comments by John Hardy

  1. Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation.
  2. Inclusion body myositis-like phenotype induced by transgenic overexpression of beta APP in skeletal muscle.
  3. Tau is essential to beta -amyloid-induced neurotoxicity.
  4. SNP association studies in Alzheimer's disease highlight problems for complex disease analysis.
  5. beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease.
  6. Prion protein protects human neurons against Bax-mediated apoptosis.
  7. A cholesterol-lowering drug reduces beta-amyloid pathology in a transgenic mouse model of Alzheimer's disease.
  8. tau Exon 10 expression involves a bipartite intron 10 regulatory sequence and weak 5' and 3' splice sites.
  9. Identification of a novel family of presenilin homologues.
  10. A lipophilic thioflavin-T derivative for positron emission tomography (PET) imaging of amyloid in brain.
  11. Determinants of 4-repeat tau expression. Coordination between enhancing and inhibitory splicing sequences for exon 10 inclusion.
  12. SNPing away at complex diseases: analysis of single-nucleotide polymorphisms around APOE in Alzheimer disease.
  13. Simvastatin strongly reduces levels of Alzheimer's disease beta -amyloid peptides Abeta 42 and Abeta 40 in vitro and in vivo.
  14. Beta-amyloid precursor protein, ETS-2 and collagen alpha 1 (VI) chain precursor, encoded on chromosome 21, are not overexpressed in fetal Down syndrome: further evidence against gene dosage effect.
  15. Reduced effectiveness of Abeta1-42 immunization in APP transgenic mice with significant amyloid deposition.