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LRRTM3 polymorphisms may play a role in the pathogenesis of late-onset Alzheimer's disease (LOAD) in a Northern Han Chinese population.
protein interactions between LRRTM3, APP and BACE1, as well as complex associations between mRNA levels of LRRTM3, CTNNA3, APP and BACE1 in humans might influence APP metabolism and ultimately risk of AD
LRRTM3 is not an essential regulator of amyloid-beta production in adult mice; there are no differences in genotype between levels of Abeta or Abeta protein precursor C-terminal fragments in vivo.
One single-nucleotide polymorphism in the promoter region and a block of 4 single-nucleotide polymorphisms in intron 2 were associated with AD in the National Institute on Aging Late-Onset Alzheimer's Disease data set or the Caribbean Hispanic data set.
Apart from the complexity of its regulation, alterations in both CTNNA3 and LRTMM3 are implicated in human disease.
Data suggest that LRRTM3 is a functional and positional candidate gene for Alzheimer disease, and, given its receptor-like structure and restricted expression, a potential therapeutic target.
An ancestral risk haplotype clade in ACE and putative multilocus association between ACE, A2M, and LRRTM3 in Alzheimer disease.
LRRTM3 is required for dentate gyrus excitatory synapse development and regulates activity-dependent AMPAR surface expression.
May play a role in the development and maintenance of the vertebrate nervous system.
leucine rich repeat transmembrane neuronal 3
, leucine-rich repeat transmembrane neuronal protein 3