ArticleCurrent neuropharmacology2013
Recent advances in the molecular pathogenesis of dystonia-plus syndromes and heredodegenerative dystonias.
Article in Current neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Oxidative stress and inflammation in the pathogenesis of neurological disorders: Mechanisms and implications.Acta pharmaceutica Sinica. B · 2025Review
- Early Onset Ataxia with Comorbid Dystonia: Clinical, Anatomical and Biological Pathway Analysis Expose Shared Pathophysiology.Diagnostics (Basel, Switzerland) · 2020Article
- Essential tremor-plus: a controversial new concept.The Lancet. Neurology · 2020Review
- A new tyrosine hydroxylase genotype with orofacial dyskinaesia.Sultan Qaboos University medical journal · 2014Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of studies investigating the molecular pathogenesis and cell biology underlying dystonia have been performed in individuals with primary dystonia. This includes monogenic forms such as DYT1and DYT6 dystonia, and primary focal dystonia which is likely to be multifactorial in origin. In recent years there has been renewed interest in non-primary forms of dystonia including the dystonia-plus syndromes and heredodegenerative disorders. These are caused by a variety of genetic mutations and their study has contributed to our understanding of the neuronal dysfunction that leads to dystonia These findings have reinforced themes identified from study of primary dystonia including abnormal dopaminergic signalling, cellular trafficking and mitochondrial function. In this review we highlight recent advances in the understanding of the dystonia-plus syndromes and heredodegenerative dystonias.
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