Luo Y, Bolon B, Kahn S, Bennett BD, Babu-Khan S, Denis P, Fan W, Kha H, Zhang J, Gong Y, Martin L, Louis JC, Yan Q, Richards WG, Citron M, Vassar R. Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation. Nat Neurosci. 2001 Mar;4(3):231-2. PubMed.

Recommends

Please login to recommend the paper.

Comments

    • User Profile Image John Hardy
      Institute of Neurology, UCL
    • Posted:

    "An excellent paper, not only establishing BACE as b -secretase but also suggesting that knockout (or, by implication drug inhibition) may not have major adverse effects."

    View all comments by John Hardy

Make a Comment

To make a comment you must login or register.

This paper appears in the following:

News

  1. β-Secretase a Clean Therapeutic Target
  2. Barcelona: Out of Left Field—Hit to The Eye Kills BACE Inhibitor
  3. 2008 MetLife Award for De Strooper, Vassar, Wong
  4. Rounding Second BACE: Another Route to Memory Loss?
  5. Target BACE: Better Than Ever?
  6. What Exactly Does BACE Do in Adults?

Webinars

  1. RNAi in Neurodegenerative Diseases—What's the Therapeutic Potential?
  2. Novel Substrates for BACE1 Beg the Question: What's the Biological Function of β-Secretase?

Research Timeline Event

  1. BACE1 knockout mice are viable