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Epigenetic suppression of neuroligin 1 underlies amyloid-induced memory deficiency.

Authors: Bie, B  Wu, J  Yang, H  Xu, JJ  Brown, DL  Naguib, M 
Citation: Bie B, etal., Nat Neurosci. 2014 Feb;17(2):223-31. doi: 10.1038/nn.3618. Epub 2014 Jan 19.
Pubmed: (View Article at PubMed) PMID:24441681
DOI: Full-text: DOI:10.1038/nn.3618

Amyloid-induced microglial activation and neuroinflammation impair central synapses and memory function, although the mechanism remains unclear. Neuroligin 1 (NLGN1), a postsynaptic protein found in central excitatory synapses, governs excitatory synaptic efficacy and plasticity in the brain. Here we found, in rodents, that amyloid fibril-induced neuroinflammation enhanced the interaction between histone deacetylase 2 and methyl-CpG-binding protein 2, leading to suppressed histone H3 acetylation and enhanced cytosine methylation in the Nlgn1 promoter region and decreased NLGN1 expression, underlying amyloid-induced memory deficiency. Manipulation of microglia-associated neuroinflammation modulated the epigenetic modification of the Nlgn1 promoter, hippocampal glutamatergic transmission and memory function. These findings link neuroinflammation, synaptic efficacy and memory, thus providing insight into the pathogenesis of amyloid-associated diseases.

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RGD Object Information
RGD ID: 9590255
Created: 2014-11-21
Species: All species
Last Modified: 2014-11-21
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.