English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Significance In human patients, mutations in theLARGE gene cause congenital muscular dystrophy (CMD) type 1D, which, unlike other types of CMD, is accompanied by severe intellectual disability. Neurological phenotypes ofLARGE knockout mice also suggest the possibility of impaired learning and memory. Our study using region-specificLARGE knockdown provides strong evidence that a deficit of LARGE in the hippocampus results in excitatory synapses being abnormally potentiated through the overloading of AMPA-type glutamate receptor, thereby impairing hippocampus-dependent memory. Our data reveal an intriguing role for LARGE in regulating the fine-tuning of synaptic strength in the hippocampus, which influences hippocampus-dependent memory. The results provide crucial insights for the therapeutic treatment of brain disorders associated with intellectual disability.

LARGE, an intellectual disability-associated protein, regulates AMPA-type glutamate receptor trafficking and memory