Evidence map›Paper›PMID 41653401›Full record

ArticleBrain imaging and behavior2026

Functional connectivity alterations in spinocerebellar ataxia type 10: insights from gray matter atrophy.

Gustavo Padron-Rivera, Gabriel Ramirez-Garcia, Amanda Chirino-Perez, Angel Omar Romero-Molina, Adriana Ochoa-Morales, María Guadalupe Garcia-Gomar, Miguel Angel Ramirez-Garcia, Omar Rodriguez-Mendoza, Diana Laura Torres-Vences, Birgitt Schüle and 3 more

Abstract read
In one paragraph

Article in Brain imaging and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

13 authors.

Gustavo Padron-Rivera *Laboratorio de Neuropsicologia, Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Mexico.
Gabriel Ramirez-Garcia *Laboratorio de Neuropsicologia, Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Mexico.
Amanda Chirino-PerezLaboratorio de Neuropsicologia, Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Mexico.
Angel Omar Romero-MolinaLaboratorio de Neuropsicologia, Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Mexico.
Adriana Ochoa-MoralesDepartamento de Neurogenetica, Instituto Nacional de Neurologia y Neurocirugia Manuel Velasco Suarez, Ciudad de Mexico, Mexico.
María Guadalupe Garcia-GomarEscuela Nacional de Estudios Superiores (ENES), Universidad Nacional Autónoma de México, Juriquilla Queretaro, Mexico.
Miguel Angel Ramirez-GarciaDepartamento de Neurogenetica, Instituto Nacional de Neurologia y Neurocirugia Manuel Velasco Suarez, Ciudad de Mexico, Mexico.
Omar Rodriguez-MendozaLaboratorio de Neuropsicologia, Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Mexico.
Diana Laura Torres-VencesLaboratorio de Neuropsicologia, Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Mexico.
Birgitt SchüleDepartment Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Erick Humberto Pasaye-AlcarazUnidad de Resonancia Magnetica, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Juriquilla Queretaro, Mexico.
Carlos Roberto Hernandez-CastilloFaculty of Computer Science, Dalhousie University, Halifax, Canada.
Juan Fernandez-RuizLaboratorio de Neuropsicologia, Departamento de Fisiologia, Facultad de Medicina, Universidad Nacional Autonoma de Mexico, Ciudad de Mexico, Mexico. jfr@unam.mx.

Funding

Consejo Nacional de Humanidades, Ciencias y Tecnologías 2272998Consejo Nacional de Humanidades, Ciencias y Tecnologías A1-S-10669Programa de Apoyo a Proyectos de Investigación e Innovación Tecnológica IN214122
6 · The paper itself

Abstract

Spinocerebellar ataxia type 10 (SCA10) is a rare, inherited neurological disease caused by an expansion of the non-coding ATTCT pentanucleotide repeat in the ATAXIN 10 gene. It is characterized by cerebellar ataxia and epilepsy. Previous research has demonstrated extensive white and gray matter degeneration, particularly in the cerebellum. However, the impact of the SCA10 mutation on functional connectivity (FC) remains unexplored. This study aimed to characterize intrinsic FC changes in SCA10 patients and their relationship to clinical manifestations. Structural and resting-state Magnetic Resonance Imaging (MRI) were obtained from 26 SCA10 patients and 26 control subjects. Voxel-based morphometry (VBM) and seed-ROI and Independent Components Analysis (ICA) were performed to identify cerebral atrophy and FC changes respectively. Additionally, correlation analyses were conducted between FC changes and scores from the Scale for the Assessment and Rating of Ataxia (SARA) and the Montreal Cognitive Assessment (MoCA). In SCA10 patients, VBM analysis revealed extensive gray matter loss in motor cortices and the cerebellum. FC analysis identified significant FC changes originating from seed-ROIs in the right cerebellar VI and left precentral gyrus. Furthermore, group comparison using ICA components showed that SCA10 patients exhibited higher FC in the sensorimotor and cerebellar functional networks. Moreover, the average Blood Oxygen Level Dependent (BOLD) signal within the cerebellar network negatively correlated with MoCA scores. In summary, SCA10 patients exhibited enhanced FC in brain regions that displayed gray matter atrophy, underscoring the impact of SCA10 degeneration on resting state networks and induction of potential maladaptive FC compensatory mechanisms.

Indexed as

BrainGray MatterSpinocerebellar AtaxiasAdultAtrophyBrain MappingCerebellumDNA Repeat ExpansionFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedNeural PathwaysCerebellumCognition.Functional connectivityGray matter atrophySpinocerebellar ataxia

Identifiers

PMID41653401
PMCPMC12882854

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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.