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

Salta, E; Sierksma, A; Vanden Eynden, E; De Strooper, B; (2016) miR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain. EMBO Molecular Medicine , 8 (9) pp. 1005-1018. 10.15252/emmm.201606520. Green open access

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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.

Type: Article
Title: miR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain
Open access status: An open access version is available from UCL Discovery
DOI: 10.15252/emmm.201606520
Publisher version: http://doi.org/10.15252/emmm.201606520
Language: English
Additional information: Copyright © 2016 The Authors. License: This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Keywords: Alzheimer’s, amyloid, ITPKB, microRNA-132, TAU
UCL classification: UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UK Dementia Research Institute HQ
URI: https://discovery.ucl.ac.uk/id/eprint/1541082
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