Unknown

Dataset Information

0

MiR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain.


ABSTRACT: microRNA-132 (miR-132) is involved in prosurvival, anti-inflammatory and memory-promoting functions in the nervous system and has been found consistently downregulated in Alzheimer's disease (AD). Whether and how miR-132 deficiency impacts AD pathology remains, however, unaddressed. We show here that miR-132 loss exacerbates both amyloid and TAU pathology via inositol 1,4,5-trisphosphate 3-kinase B (ITPKB) upregulation in an AD mouse model. This leads to increased ERK1/2 and BACE1 activity and elevated TAU phosphorylation. We confirm downregulation of miR-132 and upregulation of ITPKB in three distinct human AD patient cohorts, indicating the pathological relevance of this pathway in AD.

SUBMITTER: Salta E 

PROVIDER: S-EPMC5009807 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature

altmetric image

Publications

miR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain.

Salta Evgenia E   Sierksma Annerieke A   Vanden Eynden Elke E   De Strooper Bart B  

EMBO molecular medicine 20160901 9


microRNA-132 (miR-132) is involved in prosurvival, anti-inflammatory and memory-promoting functions in the nervous system and has been found consistently downregulated in Alzheimer's disease (AD). Whether and how miR-132 deficiency impacts AD pathology remains, however, unaddressed. We show here that miR-132 loss exacerbates both amyloid and TAU pathology via inositol 1,4,5-trisphosphate 3-kinase B (ITPKB) upregulation in an AD mouse model. This leads to increased ERK1/2 and BACE1 activity and e  ...[more]

Similar Datasets

| S-EPMC9241248 | biostudies-literature
| S-EPMC2408427 | biostudies-literature
| S-EPMC11853399 | biostudies-literature
| S-EPMC10690020 | biostudies-literature
| S-EPMC10353939 | biostudies-literature
| S-EPMC7210893 | biostudies-literature
| S-EPMC8758475 | biostudies-literature
| S-EPMC8800231 | biostudies-literature
| S-EPMC5753447 | biostudies-literature
| S-EPMC10154225 | biostudies-literature