Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation. - AlzForum Alzheimer Research Paper of the Week


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Home: Papers of the Week

Annotation

	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 Abstract, View on AlzSWAN Corresponding Author: Robert Vassar

	Comments on Paper and Primary News

	Comment by: John Hardy, ARF Advisor
	Permalink
	I recommend this paper "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

	Comment by: Yungfeng Liao
	Submitted 17 June 2004 \| Permalink	Posted 17 June 2004
	I recommend this paper

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REAGENTS/MATERIAL:

Developed BACE1-deficient mice, Tg2576 APP-overexpressing transgenic mice.

Antibodies for beta-secretase (C00 and C89) and alpha-secretase (C83). Western blot used polyclonal anti-BACE1 C-terminal antibody.

FUTURE DIRECTION:
Inhibition of BACE1 in humans may not have mechanism-based toxicity. Testing of BACE1 inhibitors in human clinical trials is needed.