LRRTM3 is Dispensable for Amyloid-β Production in Mice

Article type: Research Article

Authors: Laakso, Tiina^{a; b} | Muggalla, Pranuthi^a | Kysenius, Kai^a | Laurén, Juha^a | Paatero, Anja^a | Huttunen, Henri J.^a | Airaksinen, Matti S.^{a; b; *}

Affiliations: [a] Neuroscience Center, University of Helsinki, Helsinki, Finland | [b] Institute of Biomedicine, University of Helsinki, Helsinki, Finland

Correspondence: [*] Correspondence to: Matti S. Airaksinen, Institute of Biomedicine/Anatomy, P.O. Box 63, University of Helsinki, Helsinki 00014, Finland. E-mail: matti.airaksinen@helsinki.fi.

Abstract: Neuronal LRRTM3 (leucine-rich repeat transmembrane 3) protein has been reported to promote amyloid-β protein precursor (AβPP) processing and LRRTM3 is a candidate gene in late-onset Alzheimer's disease. To address the role of LRRTM3 in AβPP processing and amyloid-β (Aβ) production in vivo, we analyzed amyloidogenic processing of AβPP in the brains of LRRTM3-deficient mice and transgenic AβPP/PS1 mice with or without LRRTM3. We did not find differences between the genotypes in the levels of Aβ or AβPP C-terminal fragments indicating that LRRTM3 is not an essential regulator of Aβ production in adult mice. Moreover, Aβ levels in primary cortical neurons were similar between the genotypes, indicating that LRRTM3 is not required for Aβ generation in developing mice.

Keywords: Amyloid-β protein precursor, BACE1, LRR-domain, neurexin, synaptogenic

DOI: 10.3233/JAD-2012-120193

Journal: Journal of Alzheimer's Disease, vol. 31, no. 4, pp. 759-764, 2012