Evidence map›Paper›PMID 29982852›Full record

ArticleActa neuropathologica2018

MicroRNA-132 provides neuroprotection for tauopathies via multiple signaling pathways.

Rachid El Fatimy, Shaomin Li, Zhicheng Chen, Tasnim Mushannen, Sree Gongala, Zhiyun Wei, Darrick T Balu, Rosalia Rabinovsky, Adam Cantlon, Abdallah Elkhal and 4 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 3 pooled it
10.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

115 citing papers in PubMed, 3 syntheses or guidelines pooled it, 164 citations in OpenAlex.

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  20. MicroRNAs as biomarkers and molecular mediators of cognitive dysfunction in schizophrenia.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review

55 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Rachid El FatimyDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA. relfatimy@bwh.harvard.edu.
Shaomin LiDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Zhicheng ChenDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Tasnim MushannenDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Sree GongalaDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Zhiyun WeiDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Darrick T BaluDepartment of Psychiatry, McLean Hospital and Harvard Medical School, Belmont, MA, 02478, USA.
Rosalia RabinovskyDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Adam CantlonDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Abdallah ElkhalDivision of Transplant Surgery and Transplantation Surgery Research Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Dennis J SelkoeDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Kai C SonntagDepartment of Psychiatry, McLean Hospital and Harvard Medical School, Belmont, MA, 02478, USA.
Dominic M WalshDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA.
Anna M KrichevskyDepartment of Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Rd, 9006, Boston, MA, 02115, USA. akrichevsky@bwh.harvard.edu.
Brigham and Women's Hospital · USHarvard University · USHarvard Affiliated Emergency Medicine Residency · US

Funding

AGING IN THE BRAIN--ROLE OF THE FIBROUS PROTEINSR01AG006173 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI SELKOE, DENNIS J · 1985 to 2016
$2.5M
Aging in the Brain: Role of the Fibrous ProteinsRF1AG006173 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI SELKOE, DENNIS J · 2017 to 2017
$2.2M
NMDA receptor hypofunction contributes to the dendritic dysplasia in schizophreniR00MH099252 · NIMH · MCLEAN HOSPITAL · PI BALU, DARRICK T · 2015 to 2017
$726k
NMDA receptor hypofunction contributes to the dendritic dysplasia in schizophreniK99MH099252 · NIMH · MCLEAN HOSPITAL · PI BALU, DARRICK T · 2013 to 2014
$230k
Alzheimer's Association NIRG-09-132844NIA NIH HHS R01 AG006173NIA NIH HHS RF1 AG006173NIMH NIH HHS K99 MH099252NIMH NIH HHS R00 MH099252
6 · The paper itself

Abstract

MicroRNAs (miRNA) regulate fundamental biological processes, including neuronal plasticity, stress response, and survival. Here, we describe a neuroprotective function of miR-132, the miRNA most significantly downregulated in neurons in Alzheimer's disease. We demonstrate that miR-132 protects primary mouse and human wild-type neurons and more vulnerable Tau-mutant neurons against amyloid β-peptide (Aβ) and glutamate excitotoxicity. It lowers the levels of total, phosphorylated, acetylated, and cleaved forms of Tau implicated in tauopathies, promotes neurite elongation and branching, and reduces neuronal death. Similarly, miR-132 attenuates PHF-Tau pathology and neurodegeneration, and enhances long-term potentiation in the P301S Tau transgenic mice. The neuroprotective effects are mediated by direct regulation of the Tau modifiers acetyltransferase EP300, kinase GSK3β, RNA-binding protein Rbfox1, and proteases Calpain 2 and Caspases 3/7. These data suggest miR-132 as a master regulator of neuronal health and indicate that miR-132 supplementation could be of therapeutic benefit for the treatment of Tau-associated neurodegenerative disorders.

Indexed as

Amyloid beta-PeptidesAnimalsCell DeathGlutamic AcidHumansMiceMice, TransgenicMicroRNAsMutationNerve DegenerationNeuritesNeuronsPrimary Cell CultureProtein Processing, Post-TranslationalRNA, Long NoncodingSignal TransductionAmyloid beta-PeptidesGlutamic AcidMicroRNAsMIRN132 microRNA, humanMIRN132 microRNA, mouseRNA, Long Noncodingtau ProteinsAlzheimer’s diseaseMicroRNANeurodegenerationNeuroprotectionNon-coding RNATauopathies

Identifiers

PMID29982852
PMCPMC6132948
OpenAlexW2949187527

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.