Evidence map›Paper›PMID 32448329›Full record

ArticleMolecular neurodegeneration2020

Interleukin-6 deficiency exacerbates Huntington's disease model phenotypes.

Mary H Wertz, S Sebastian Pineda, Hyeseung Lee, Ruth Kulicke, Manolis Kellis, Myriam Heiman

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Interleukin-6, CD8Frontiers in aging neuroscience · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Mary H WertzPicower Institute for Learning and Memory, Cambridge, MA, 02139, USA.
S Sebastian PinedaBroad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.
Hyeseung LeePicower Institute for Learning and Memory, Cambridge, MA, 02139, USA.
Ruth KulickePicower Institute for Learning and Memory, Cambridge, MA, 02139, USA.
Manolis KellisBroad Institute of MIT and Harvard, Cambridge, MA, 02142, USA.
Myriam HeimanDepartment of Brain and Cognitive Sciences, MIT, Cambridge, MA, 02139, USA. mheiman@mit.edu.
Broad Institute · US

Funding

Epigenomic, transcriptional and cellular dissection of Alzheimer's variantsR01AG058002 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HYMAN, BRADLEY T., JAENISCH, RUDOLF · 2017 to 2021
$7.9M
Single-cell transcriptional and epigenomic dissection of Alzheimer's Disease and Related DementiasU01NS110453 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KELLIS, MANOLIS, TSAI, LI-HUEI · 2018 to 2020
$4.0M
Construction of an integrated immune - vascular brain - chip as a platform for the study, drug screening, and treatments of Alzheimer's diseaseUG3NS115064 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BLANCHARD, JOEL WILLIAM, KELLIS, MANOLIS · 2019 to 2020
$2.5M
Development of SLIC, a methodology for synthetic lethal screening in the CNSR01NS085880 · NINDS · BROAD INSTITUTE, INC. · PI HEIMAN, MYRIAM · 2013 to 2016
$1.4M
Supplement to Neurobiological Engineering Training ProgramT32EB019940 · NIBIB · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI JASANOFF, ALAN · 2015 to 2025
$1.4M
NIA NIH HHS R01 AG058002NIBIB NIH HHS T32 EB019940NINDS NIH HHS R01 NS085880NINDS NIH HHS U01 NS110453NINDS NIH HHS UG3 NS115064
6 · The paper itself

Abstract

Huntington's disease (HD) is an incurable neurodegenerative disorder caused by CAG trinucleotide expansions in the huntingtin gene. Markers of both systemic and CNS immune activation and inflammation have been widely noted in HD and mouse models of HD. In particular, elevation of the pro-inflammatory cytokine interleukin-6 (IL-6) is the earliest reported marker of immune activation in HD, and this elevation has been suggested to contribute to HD pathogenesis. To test the hypothesis that IL-6 deficiency would be protective against the effects of mutant huntingtin, we generated R6/2 HD model mice that lacked IL-6. Contrary to our prediction, IL-6 deficiency exacerbated HD-model associated behavioral phenotypes. Single nuclear RNA Sequencing (snRNA-seq) analysis of striatal cell types revealed that IL-6 deficiency led to the dysregulation of various genes associated with synaptic function, as well as the BDNF receptor Ntrk2. These data suggest that IL-6 deficiency exacerbates the effects of mutant huntingtin through dysregulation of genes of known relevance to HD pathobiology in striatal neurons, and further suggest that modulation of IL-6 to a level that promotes proper regulation of genes associated with synaptic function may hold promise as an HD therapeutic target.

Indexed as

PhenotypeAnimalsBrainCorpus StriatumDisease Models, AnimalHuntington DiseaseInterleukin-6Mice, TransgenicInterleukin-6Huntington’s diseaseInterleukin-6snRNA-seq

Identifiers

PMID32448329
PMCPMC7247164
OpenAlexW3028059710

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.