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Experimental Genetics Group

Bolleke Abstract   Pijltje
Beta-site amyloid precursor protein-cleaving enzyme-1 (BACE1)-mediated changes of endogenous amyloid beta in wild-type and transgenic mice in vivo.

Neurosci Lett. 2008 Apr 25;435(3):186-9.

Hirata-Fukae C1, Sidahmed EH1, Gooskens TP1, Aisen PS1,2, Dewachter I3, Devijver H3, Van Leuven F3, Matsuoka Y1*.

1Department of Neurology, Georgetown University Medical Center, Washington, DC, USA.
2Alzheimer's Disease Cooperative Study, Department of Neurosciences, University of California San Diego, San Diego, CA, USA.
3Experimental Genetics Group, Department of Human Genetics, K.U.Leuven, Leuven, Belgium.
*Corresponding author.

Beta-site amyloid precursor protein-cleaving enzyme-1 (BACE1) initiates generation of amyloid beta (Abeta), a pathological hallmark of Alzheimer's disease. We investigated the impact of BACE1 protein level on endogenous Abeta. Endogenous Abeta and BACE1 protein levels were concurrently and significantly reduced during early life. However, Abeta levels were similar between BACE1 transgenic and wildtype mice. This suggests that BACE1 protein level has a minimal effect on the level of endogenous Abeta. Consequently, other factors must be involved in modulation of Abeta production in adult and ageing brain and investigation of such factors may yield therapeutic targets. Further, these results suggest that substantial inhibition of BACE1 in brain may be required for clinical benefit in Alzheimer's disease.

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