Evidence map›Paper›PMID 21969577›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2011

Transcriptional modulator H2A histone family, member Y (H2AFY) marks Huntington disease activity in man and mouse.

Yi Hu, Vanita Chopra, Raman Chopra, Joseph J Locascio, Zhixiang Liao, Hongliu Ding, Bin Zheng, Wayne R Matson, Robert J Ferrante, H Diana Rosas and 2 more

Open access · greenAbstract readClinical Trial, Phase IIMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  16. A Glimpse of Molecular Biomarkers in Huntington's Disease.International journal of molecular sciences · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 7 institutions in 1 country.

Yi HuLaboratory for Neurogenomics, Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Cambridge, MA 02139, USA.
Vanita Chopra
Raman Chopra
Joseph J Locascio
Zhixiang Liao
Hongliu Ding
Bin Zheng
Wayne R Matson
Robert J Ferrante
H Diana Rosas
Steven M Hersch
Clemens R Scherzer
Brigham and Women's Hospital · USMaineGeneral Medical Center · USMassachusetts General Hospital · USAthinoula A. Martinos Center for Biomedical Imaging · USGeriatric Research Education and Clinical Center · USHarvard University · USUniversity of Pittsburgh · US

Funding

Neuroimaging Biomarkers for disease-modyfying therapies in Hintington's diseaseP01NS058793 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI HERSCH, STEVEN M · 2008 to 2012
$6.6M
Transcription and Therapy for HD: from Molecules to ManP01NS045242 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI KRAINC, DIMITRI · 2003 to 2007
$6.3M
Prospective Neuroimaging in Huntington's DiseaseR01NS042861 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAS, HERMINIA DIANA · 2003 to 2013
$5.6M
Risk Marker for Parkinson's Disease: Enabling Novel TherapiesR01NS064155 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SCHERZER, CLEMENS R · 2008 to 2011
$1.7M
Multigene Marker of Progression in Parkinson's DiseaseR21NS060227 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SCHERZER, CLEMENS R · 2007 to 2008
$421k
NINDS NIH HHS P01 NS045242NINDS NIH HHS P01NS045242NINDS NIH HHS P01 NS058793NINDS NIH HHS P01NS058793NINDS NIH HHS R01 NS042861NINDS NIH HHS R01NS042861NINDS NIH HHS R01 NS064155NINDS NIH HHS R01NS064155NINDS NIH HHS R21 NS060227NINDS NIH HHS R21NS060227
6 · The paper itself

Abstract

Huntington disease (HD) is a progressive neurodegenerative disease that affects 30,000 individuals in North America. Treatments that slow its relentless course are not yet available, and biomarkers that can reliably measure disease activity and therapeutic response are urgently needed to facilitate their development. Here, we interrogated 119 human blood samples for transcripts associated with HD. We found that the dynamic regulator of chromatin plasticity H2A histone family, member Y (H2AFY) is specifically overexpressed in the blood and frontal cortex of patients with HD compared with controls. This association precedes the onset of clinical symptoms, was confirmed in two mouse models, and was independently replicated in cross-sectional and longitudinal clinical studies comprising 142 participants. A histone deacetylase inhibitor that suppresses neurodegeneration in animal models reduces H2AFY levels in a randomized phase II clinical trial. This study identifies the chromatin regulator H2AFY as a potential biomarker associated with disease activity and pharmacodynamic response that may become useful for enabling disease-modifying therapeutics for HD.

Indexed as

AdultAgedAnimalsCase-Control StudiesCross-Sectional StudiesDisease Models, AnimalDouble-Blind MethodFemaleFrontal LobeGene ExpressionHistone Deacetylase InhibitorsHistonesHumansHuntington DiseaseLongitudinal StudiesMaleHistone Deacetylase InhibitorsHistonesMACROH2A2 protein, humanmacroH2A histoneRNA, Messenger

Identifiers

PMID21969577
PMCPMC3193232
OpenAlexW2060873702

What OpenQuestion holds

Textmetadata
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.