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Maria Spadaro

Researcher at Sapienza University of Rome

Publications -  40
Citations -  2181

Maria Spadaro is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: Cerebellar ataxia & Ataxia. The author has an hindex of 20, co-authored 40 publications receiving 2032 citations. Previous affiliations of Maria Spadaro include National Research Council.

Papers
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Journal Article

Correlation between morphological and functional retinal impairment in multiple sclerosis patients.

Vincenzo Parisi, +7 more
- 01 Oct 1999 - 
TL;DR: There is a correlation between PERG changes and NFL thickness in MS patients previously affected by optic neuritis, but there is no correlation between VEP changes andNFL thickness.
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Episodic Ataxia Type 2 (EA2) and Spinocerebellar Ataxia Type 6 (SCA6) Due to CAG Repeat Expansion in the CACNA1A Gene on Chromosome 19p

Carla Jodice, +12 more
- 01 Oct 1997 - 
TL;DR: The results show that EA2 and SCA6 are the same disorder with a high phenotypic variability, at least partly related to the number of repeats, and suggest that the small CAG expansions may not be as stable as previously reported.
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Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Davina J. Hensman Moss, +734 more
- 01 Sep 2017 - 
TL;DR: A novel measure of disease progression and a genome-wide significant signal on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2 is generated, suggesting this mechanism as an area for future therapeutic investigation.
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Riluzole in patients with hereditary cerebellar ataxia: a randomised, double-blind, placebo-controlled trial

Silvia Romano, +15 more
- 01 Oct 2015 - 
TL;DR: The findings lend support to the idea that riluzole could be a treatment for cerebellar ataxia, and longer studies and disease-specific trials are needed to confirm whether these findings can be applied in clinical practice.
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Complete loss of P/Q calcium channel activity caused by a CACNA1A missense mutation carried by patients with episodic ataxia type 2.

Serena Guida, +15 more
- 01 Mar 2001 - 
TL;DR: It is indicated that a complete loss of P/Q channel function is the mechanism underlying EA2, whether due to truncating or to missense mutations.