# Targeting Cognitive Dysfunction in Spinocerebellar Ataxia Type 2 Through Digital Cognitive Training

**Authors:** Andressa Aline Vieira, Renata Barreto Tenório, Salmo Raskin, Karla Patricia Figueroa, Stefan M Pulst, Amer Cavalheiro Handam, Hélio Afonso Ghizoni Teive, Carlos Henrique Ferreira Camargo

PMC · DOI: 10.1007/s12311-025-01956-2 · Cerebellum (London, England) · 2026-03-02

## TL;DR

This study shows that digital cognitive training can improve memory in patients with Spinocerebellar Ataxia Type 2, a neurodegenerative disorder.

## Contribution

The study is the first to evaluate the effects of a digital cognitive training program on cognitive functions in SCA2 patients.

## Key findings

- SCA2 patients showed significant cognitive impairments in memory, attention, and executive functions compared to healthy controls.
- Digital cognitive training led to significant improvements in memory subcomponents like incidental and delayed memory.
- Executive functions showed limited or no improvement following the training intervention.

## Abstract

Background: Spinocerebellar ataxia type 2 (SCA2) is a neurodegenerative disorder characterized not only by motor impairment but also by significant cognitive decline. While cognitive training programs have shown promising results in other neurological conditions, evidence regarding their efficacy in SCA2 remains scarce. Objective: To assess cognitive performance in patients with SCA2 and to evaluate the impact of a digital cognitive training program on cognitive functions. Methods: Twelve SCA2 patients (50% male; 46 ± 11.51 years old; 8 ± 3.69 years of education) underwent a comprehensive neuropsychological assessment before and after a six-month cognitive training program delivered through the NeuroNation® digital platform. The evaluated cognitive functions included memory, executive function, language, complex attention, and perceptual–motor abilities. A control group of 12 healthy individuals from the community was selected and matched for sex, age, and education (50% male; 47 ± 11.68 years old; 8 ± 3.85 years of education). Results: SCA2 patients exhibited significantly lower performance across multiple cognitive functions compared to controls, with marked impairments in verbal and visual memory, verbal fluency, attention, and executive function. Following the intervention, significant improvements were observed in several memory subcomponents, including incidental, immediate, delayed, and recognition memory. However, changes in executive functions were limited or absent. No strong correlations were found between game difficulty level and neuropsychological test outcomes. Conclusion: SCA2 patients demonstrated significant cognitive impairments, particularly in memory-related functions, and responded to digital cognitive training. These findings suggest the potential role of targeted interventions in supporting cognitive function in SCA2.

The online version contains supplementary material available at 10.1007/s12311-025-01956-2.

## Linked entities

- **Diseases:** Spinocerebellar Ataxia Type 2 (MONDO:0008458)

## Full-text entities

- **Genes:** ATXN2 (ataxin 2) [NCBI Gene 6311] {aka ATX2, SCA2, TNRC13}
- **Diseases:** CCAS (MESH:D002526), Barkley Deficits in Executive (MESH:D009461), Verbal memory impairment (MESH:D008569), motor impairment (MESH:D000068079), Cognitive Dysfunction (MESH:D003072), depression (MESH:D003866), speech disturbance (MESH:D013064), degeneration (MESH:D009410), executive dysfunction (MESH:D006331), oculomotor disturbances (MESH:D015840), personality disturbances (MESH:D010554), SCA (MESH:C565772), impairments in verbal memory, visuospatial (MESH:D000377), dysarthria (MESH:D004401), cognitive fatigue (MESH:D005221), SCA2 (MESH:D020754), Barkley Deficits in Executive Functioning (MESH:D001289), psychotic (MESH:D011618), COVID-19 (MESH:D000086382), behavioral disturbances (MESH:D001523), neurocognitive decline (MESH:D060825), Hospital Anxiety and Depression (MESH:D001007), motor incoordination (MESH:D002524), neurodegenerative disorder (MESH:D019636), PD (MESH:D010300), died (MESH:D003643), Ataxia (MESH:D001259), sleep disturbances (MESH:D012893)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12953462/full.md

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Source: https://tomesphere.com/paper/PMC12953462