Evidence map›Paper›PMID 41437984›Full record

ReviewBrain, behavior, & immunity - health2025

Animal models of Huntington's disease. Pros and cons.

Polina Stepanova, Merja H Voutilainen, Ove Eriksson, Dan Lindholm

Erratum issuedAbstract readReview
In one paragraph

Review in Brain, behavior, & immunity - health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Polina StepanovaFaculty of Pharmacy, University of Helsinki, Helsinki, Finland.
Merja H VoutilainenFaculty of Pharmacy, University of Helsinki, Helsinki, Finland.
Ove ErikssonMedicum, Department of Biochemistry and Developmental Biology, Medical Faculty, POB 63, FIN-00014, University of Helsinki, Finland.
Dan LindholmMedicum, Department of Biochemistry and Developmental Biology, Medical Faculty, POB 63, FIN-00014, University of Helsinki, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Modelling of human neurological diseases uses a plethora of ever-more sophisticated methods and approaches. For Huntington's disease (HD), which affects specific neuronal types and circuits in the brain, this has meant the use of both neurotoxic compounds and various animal models of different complexity, ranging from rodents to non-primate ones. Genetic models are classified based on the use of specific constructs including gene including gene fragments, full-length, knock-out and knock-in models. In this review, we will discuss the available animal models for HD, highlighting their pros and cons in studying the neuropathology, behavioural alterations, and biological mechanisms that prevail in HD and during the disease progression. We also highlight present knowledge gaps and difficulties to fully recapitulate the human disease. At the end we will further elaborate on current outstanding questions in HD research that warrant further studies using both animal models and patient data. This may help to guide future research and increase the translational relevance of the models to solve key questions and pave the way for better treatment options and design of drugs to alleviate the course of HD.

Indexed as

Genetic modelsHuntington's diseaseNeurodegenerationNeuroinflammationNeurotoxinNon-human primateRodentSex differences

Identifiers

PMID41437984
PMCPMC12721061

What Socratic 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 Socratic graph.