Evidence map›Paper›PMID 40542543›Full record

ArticleJournal of neurochemistry2025

Increased Activity-Dependent Bulk Endocytosis in Huntington's Disease Results From Huntingtin Haploinsufficiency.

Han C G Tan, Robyn L McAdam, Andrew Morton, Michael A Cousin, Karen J Smillie

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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

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

5 authors.

Han C G TanCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, Edinburgh, Scotland, UK.ORCID 0009-0007-8952-2073
Robyn L McAdamCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, Edinburgh, Scotland, UK.
Andrew MortonCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, Edinburgh, Scotland, UK.
Michael A CousinCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, Edinburgh, Scotland, UK.ORCID 0000-0002-1762-160X
Karen J SmillieCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, Edinburgh, Scotland, UK.ORCID 0000-0003-4369-0470

Funding

Biotechnology and Biological Sciences Research CouncilCure Huntington's Disease Initiative A-11210Cure Huntington's Disease Initiative A-4390
6 · The paper itself

Abstract

Huntington's disease (HD) is a life-limiting, progressive monogenic neurodegenerative disorder characterised by chorea, hypokinesis and psychosocial symptoms. HD is characterised by a variable CAG expansion in exon 1 of the HTT gene, which encodes the huntingtin (htt) protein. This expansion results in an extended polyglutamine tract, which is widely thought to confer a toxic gain of function on the protein that is responsible for disease progression. Most individuals with HD are heterozygous for this mutation, meaning that loss of wild-type htt function may also contribute to disease pathology. We previously identified that the recycling of synaptic vesicle proteins at the presynapse was specifically disrupted in striatal neurons from a preclinical model of HD, the Htt

Indexed as

EndocytosisHaploinsufficiencyHuntingtin ProteinHuntington DiseaseAnimalsHumansMaleMiceMice, Inbred C57BLMice, TransgenicNeuronsHtt protein, mouseHuntingtin ProteinendocytosishaploinsufficiencyHuntington's diseasemousepresynapsesynaptic vesicle

Identifiers

PMID40542543
PMCPMC12181757

What OpenQuestion holds

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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.