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Roberto Rodríguez-Labrada

Researcher at University of Holguín

Publications -  69
Citations -  1370

Roberto Rodríguez-Labrada is an academic researcher from University of Holguín. The author has contributed to research in topics: Spinocerebellar ataxia & Ataxia. The author has an hindex of 19, co-authored 63 publications receiving 1081 citations.

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Preliminary evaluation of the effect of Compvit-B on memory and learning processes in patients with SCA2

TL;DR: Additional evidence is provided in support of the therapeutic and neuroprotective use of B-complex vitamins and a new option of symptomatic treatment for patients with SCA2 is presented, which will lead to an improvement in their quality of life.
Book ChapterDOI

Eye Movement Abnormalities in Neurodegenerative Diseases

TL;DR: The state of the art of the eye movement's deficits in some neurodegenerative diseases, such as Parkinson’s disease, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington’S disease, and the hereditary ataxias are reviewed.
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Recessive Spinocerebellar Ataxia with Paroxysmal Cough Attacks: A Report of Five Cases

TL;DR: Clinical criteria and molecular genetic testing suggest the presence of a new form of recessive ataxia, in which cerebellar signs are preceded by paroxysmal cough, which affects not only the cerebellum and its fiber connections, but also the sensory peripheral nervous system and extracerebellar central pathways.
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Involvement of the Auditory Pathway in Spinocerebellar Ataxia Type 7.

TL;DR: In this article, the brainstem auditory-evoked potentials (BAEPs) were assessed in 12 SCA7 patients with clinical and molecular diagnosis, compared to 2 control groups of 16 SCA2 patients and 16 healthy controls.
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One‑carbon metabolism factor MTHFR variant is associated with saccade latency in Spinocerebellar Ataxia type 2.

TL;DR: Evidence is provided that folate-mediated one-carbon metabolism might be important in the physiopathology of SCA2, following up on recent genome-wide association analyses that demonstrated the prominent role of DNA-damage repair and methylation for the severity and progression of polyglutamine diseases.