LRRTM3 is Dispensable for Amyloid-β Production in Mice

被引:6
|
作者
Laakso, Tiina [2 ]
Muggalla, Pranuthi
Kysenius, Kai
Lauren, Juha
Paatero, Anja
Huttunen, Henri J.
Airaksinen, Matti S. [1 ,2 ]
机构
[1] Univ Helsinki, Inst Biomed Anat, Ctr Neurosci, FIN-00014 Helsinki, Finland
[2] Univ Helsinki, Inst Biomed, FIN-00014 Helsinki, Finland
基金
芬兰科学院;
关键词
Amyloid-beta protein precursor; BACE1; LRR-domain; neurexin; synaptogenic; EXCITATORY SYNAPSE FORMATION; ONSET ALZHEIMERS-DISEASE; BACE1; PROTEIN; GENE; CHROMOSOME-10; ASSOCIATION; SECRETASE; LINKAGE; SYSTEM;
D O I
10.3233/JAD-2012-120193
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neuronal LRRTM3 (leucine-rich repeat transmembrane 3) protein has been reported to promote amyloid-beta protein precursor (A beta PP) processing and LRRTM3 is a candidate gene in late-onset Alzheimer's disease. To address the role of LRRTM3 in A beta PP processing and amyloid-beta (A beta) production in vivo, we analyzed amyloidogenic processing of A beta PP in the brains of LRRTM3-deficient mice and transgenic A beta PP/PS1 mice with or without LRRTM3. We did not find differences between the genotypes in the levels of A beta or A beta PP C-terminal fragments indicating that LRRTM3 is not an essential regulator of A beta production in adult mice. Moreover, A beta levels in primary cortical neurons were similar between the genotypes, indicating that LRRTM3 is not required for A beta generation in developing mice.
引用
收藏
页码:759 / 764
页数:6
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