Evidence map›Paper›PMID 30913220›Full record

ArticlePloS one2019

Meso scale discovery-based assays for the detection of aggregated huntingtin.

Wolfgang Reindl, Barbara Baldo, Jana Schulz, Isabell Janack, Ilka Lindner, Markus Kleinschmidt, Yalda Sedaghat, Christina Thiede, Karsten Tillack, Christina Schmidt and 12 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.5field-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

32 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
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  10. Preclinical evaluation of the novel [European journal of nuclear medicine and molecular imaging · 2024
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  20. Deletion of SUMO1 attenuates behavioral and anatomical deficits by regulating autophagic activities in Huntington disease.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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

22 authors at 3 institutions in 3 countries.

Wolfgang ReindlEvotec AG, Hamburg, Germany.
Barbara BaldoEvotec AG, Hamburg, Germany.
Jana SchulzEvotec AG, Hamburg, Germany.
Isabell JanackEvotec AG, Hamburg, Germany.
Ilka LindnerEvotec AG, Hamburg, Germany.
Markus KleinschmidtEvotec AG, Hamburg, Germany.
Yalda SedaghatEvotec AG, Hamburg, Germany.
Christina ThiedeEvotec AG, Hamburg, Germany.
Karsten TillackEvotec AG, Hamburg, Germany.
Christina SchmidtEvotec AG, Hamburg, Germany.
Isabell CardaunEvotec AG, Hamburg, Germany.
Tom SchwagarusEvotec AG, Hamburg, Germany.
Frank HerrmannEvotec AG, Hamburg, Germany.
Madlen HotzeEvotec AG, Hamburg, Germany.
Georgina F OsborneDept. Neurodegenerative Disease, Huntington's Disease Centre and Dementia Research Institute, Institute of Neurology, University College London, London, United Kingdom.ORCID 0000-0001-8308-3179
Simone HerrmannEvotec AG, Hamburg, Germany.
Andreas WeissEvotec AG, Hamburg, Germany.
Celina ZerbinattiEvotec AG, Hamburg, Germany.
Gillian P BatesDept. Neurodegenerative Disease, Huntington's Disease Centre and Dementia Research Institute, Institute of Neurology, University College London, London, United Kingdom.
Jonathan BardCHDI Management/CHDI Foundation, Los Angeles, CA, United States of America.
Ignacio Munoz-SanjuanCHDI Management/CHDI Foundation, Los Angeles, CA, United States of America.
Douglas MacdonaldCHDI Management/CHDI Foundation, Los Angeles, CA, United States of America.ORCID 0000-0001-5592-5594
Evotec (Germany) · DECHDI Foundation · USUK Dementia Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a monogenic neurodegenerative disorder caused by an expansion of the CAG trinucleotide repeat domain in the huntingtin (HTT) gene, leading to an expanded poly-glutamine (polyQ) stretch in the HTT protein. This mutant HTT (mHTT) protein is highly prone to intracellular aggregation, causing significant damage and cellular loss in the striatal, cortical, and other regions of the brain. Therefore, modulation of mHTT levels in these brain regions in order to reduce intracellular mHTT and aggregate levels represents a direct approach in the development of HD therapeutics. To this end, assays that can be used to detect changes in HTT levels in biological samples are invaluable tools to assess target engagement and guide dose selection in clinical trials. The Meso Scale Discovery (MSD) ELISA-based assay platform is a robust and sensitive method previously employed for the quantification of HTT. However, the currently available MSD assays for HTT are primarily detecting the monomeric soluble form of the protein, but not aggregated species. In this study, we describe the development of novel MSD assays preferentially detecting mHTT in an aggregated form. Recombinant monomeric HTT(1-97)-Q46, which forms aggregates in a time-dependent manner, was used to characterize the ability of each established assay to distinguish between HTT monomers and HTT in a higher assembly state. Further validation of these assays was performed using brain lysates from R6/2, zQ175 knock-in, and BACHD mouse models, to replicate a previously well-characterized age-dependent increase in brain aggregate signals, as well as a significant reduction of aggregate levels in the striatum following mHTT knockdown with a CAG-directed allele-specific zinc-finger repressor protein (ZFP). Lastly, size exclusion chromatography was used to separate and characterize HTT species from brain tissue lysates to demonstrate specificity of the assays for the fractions containing aggregated HTT. In summary, we demonstrate that the newly developed assays preferentially detect aggregated HTT with improved performance in comparison to previous assay technologies. These assays complement the existing MSD platform assays specific for soluble HTT monomers, allowing for a more comprehensive analysis of disease-relevant HTT species in preclinical models of HD.

Indexed as

Biological AssayAnimalsBrainDisease Models, AnimalHumansHuntingtin ProteinHuntington DiseaseMiceMice, TransgenicPeptidesProtein Aggregation, PathologicalHTT protein, humanHuntingtin ProteinPeptidespolyglutamine

Identifiers

PMID30913220
PMCPMC6435127
OpenAlexW2923035979

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.