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Claudia B. Catarino

Researcher at Ludwig Maximilian University of Munich

Publications -  53
Citations -  4037

Claudia B. Catarino is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Epilepsy & Leber's hereditary optic neuropathy. The author has an hindex of 24, co-authored 47 publications receiving 3202 citations. Previous affiliations of Claudia B. Catarino include Epilepsy Society & UCL Institute of Neurology.

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Analysis of shared heritability in common disorders of the brain

Verneri Anttila, +720 more
- 22 Jun 2018 - 
TL;DR: It is demonstrated that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine, and it is shown that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures.
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Genome-wide mega-analysis identifies 16 loci and highlights diverse biological mechanisms in the common epilepsies

Bassel Abou-Khalil, +158 more
TL;DR: The authors perform genome-wide association studies for 3 broad and 7 subtypes of epilepsy and identify 16 loci - 11 novel - that are further annotated by eQTL and partitioned heritability analyses that provide leads for epilepsy therapies based on underlying pathophysiology.
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Genetic determinants of common epilepsies: a meta-analysis of genome-wide association studies

Richard Anney, +111 more
- 30 Jul 2014 - 
TL;DR: This meta-analysis describes a new locus not previously implicated in epilepsy and provides further evidence about the genetic architecture of these disorders, with the ultimate aim of assisting in disease classification and prognosis.
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Rare deletions at 16p13.11 predispose to a diverse spectrum of sporadic epilepsy syndromes.

TL;DR: Genome-wide screens to identify copy number variation in patients with a diverse spectrum of epilepsy syndromes and in neurologically-normal controls implicate 16p13.11 and possibly other large deletions as risk factors for a wide range of epilepsy disorders, and they appear to point toward haploinsufficiency as a contributor to the pathogenicity of deletions.