Evidence map›Paper›PMID 41071260›Full record

ArticleCerebellum (London, England)2025

Cognitive Deficits in Spinocerebellar Ataxia Type 2: A Comparative Analysis of Pre-ataxic and Ataxic Stages.

Renata Barreto Tenorio, Andressa Aline Vieira, Walter Oleschko Arruda, Gustavo Leite Franklin, Gustavo da Cunha Ribas, João Filipe de Oliveira, Salmo Raskin, Karla Pattie Figueroa, Stefan M Pulst, Hélio Afonso Ghizoni Teive and 1 more

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Cerebellum (London, England), 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

11 authors.

Renata Barreto TenorioNeurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department, Hospital de Clínicas, Federal University of Paraná, Rua General Osório, 181, 10º andar - PPGMICS, 80060-000, Curitiba, Paraná, Brazil. genetica.curitiba@gmail.com.ORCID http://orcid.org/0000-0002-4802-9430
Andressa Aline VieiraNeurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department, Hospital de Clínicas, Federal University of Paraná, Rua General Osório, 181, 10º andar - PPGMICS, 80060-000, Curitiba, Paraná, Brazil.ORCID http://orcid.org/0009-0001-2821-0021
Walter Oleschko ArrudaMovement Disorders Sector, Neurology Service, Internal Medicine Department, Hospital de Clínicas, Federal University of Paraná, Curitiba, Paraná, Brazil.ORCID http://orcid.org/0000-0002-2233-2183
Gustavo Leite FranklinNeurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department, Hospital de Clínicas, Federal University of Paraná, Rua General Osório, 181, 10º andar - PPGMICS, 80060-000, Curitiba, Paraná, Brazil.ORCID http://orcid.org/0000-0002-0207-3671
Gustavo da Cunha RibasNeurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department, Hospital de Clínicas, Federal University of Paraná, Rua General Osório, 181, 10º andar - PPGMICS, 80060-000, Curitiba, Paraná, Brazil.ORCID http://orcid.org/0000-0003-1997-0552
João Filipe de OliveiraNeurology Sector,, Department of Internal Medicine, Santa Isabel Hospital, Blumenau, Santa Catarina, Brazil.ORCID http://orcid.org/0000-0001-6059-7652
Salmo RaskinGenetika - Genetic Counseling Center and Laboratory, Curitiba, Paraná, Brazil.ORCID http://orcid.org/0000-0002-7191-0592
Karla Pattie FigueroaDepartment of Neurology, University of Utah, Salt Lake City, UT, USA.ORCID http://orcid.org/0000-0003-4857-9288
Stefan M PulstDepartment of Neurology, University of Utah, Salt Lake City, UT, USA.ORCID http://orcid.org/0000-0003-0883-7879
Hélio Afonso Ghizoni TeiveNeurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department, Hospital de Clínicas, Federal University of Paraná, Rua General Osório, 181, 10º andar - PPGMICS, 80060-000, Curitiba, Paraná, Brazil.ORCID http://orcid.org/0000-0003-2305-1073
Carlos Henrique Ferreira CamargoNeurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department, Hospital de Clínicas, Federal University of Paraná, Rua General Osório, 181, 10º andar - PPGMICS, 80060-000, Curitiba, Paraná, Brazil.ORCID http://orcid.org/0000-0002-3533-0347

Funding

Ataxin-2 complex proteins in neurodegeneration.R35NS127253 · NINDS · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Stefan M. PULST · 2022 to 2026
$4.6M
NIH HHS R35NS127253NINDS NIH HHS R35 NS127253
6 · The paper itself

Abstract

Spinocerebellar ataxia type 2 (SCA2) is a neurodegenerative disorder characterized by cerebellar motor symptoms. The extent and timing of cognitive involvement, particularly in pre-ataxic carriers, remain unclear. To assess cognitive performance across clinical stages of SCA2 and investigate early neurocognitive changes in pre-ataxic individuals. We evaluated 52 genetically confirmed participants from a rural Brazilian cohort: 16 pre-ataxic carriers, 12 symptomatic patients, and 24 intrafamilial controls. A standardized neuropsychological battery assessed global cognition, executive function, memory, visuospatial abilities, attention/working memory, mood, and language. Group comparisons and correlations were adjusted using False Discovery Rate (FDR) correction. Pre-ataxic carriers performed comparably to their intrafamilial controls across all cognitive domains, with no significant group differences except for the FAB total score, and showed no associations with estimated time to disease onset. Executive dysfunction emerged as the most prominent cognitive feature of manifest SCA2 and was more strongly associated with CAG repeat length than with clinical disease markers. In this genetically and environmentally homogeneous cohort, only limited measurable cognitive impairment was observed in pre-ataxic carriers. These findings underscore the importance of longitudinal and multimodal studies to elucidate the timing and underlying mechanisms of cognitive decline in SCA2.

Indexed as

Cognitive DysfunctionSpinocerebellar AtaxiasAdultCohort StudiesExecutive FunctionFemaleHumansMaleMiddle AgedNeuropsychological TestsCAG repeatCognitive impairmentExecutive functionNeuropsychologyPreclinical cognitionSpinocerebellar ataxia type 2

Identifiers

PMID41071260
PMCPMC12990888

What OpenQuestion holds

Textmetadata
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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.