Research ArticleNeuroscience

Differential splicing and glycosylation of Apoer2 alters synaptic plasticity and fear learning

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Science Signaling  25 Nov 2014:
Vol. 7, Issue 353, pp. ra113
DOI: 10.1126/scisignal.2005438

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Sugar for Normal Brain Function

Alzheimer’s disease is a neurodegenerative disorder that results in dementia. Decreased signaling through the receptor Apoer2 exacerbates some of the molecular changes that occur in Alzheimer’s disease. Wasser et al. generated mice with a form of Apoer2 lacking the domain that is heavily glycosylated with O-linked sugars. The abundance of this mutant receptor in these mice was higher than that of Apoer2 in wild-type mice. Lack of this domain resulted in changes in synaptic morphology and composition, decreased synaptic efficacy, and defects in learning and memory. These neurological effects appeared to depend on the increased amount of the mutant receptor because they were absent in mice with lower amounts of the mutant receptor.

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