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Olaf Ansorge

Researcher at University of Oxford

Publications -  9
Citations -  1465

Olaf Ansorge is an academic researcher from University of Oxford. The author has contributed to research in topics: Dementia with Lewy bodies & Genome-wide association study. The author has an hindex of 8, co-authored 9 publications receiving 1264 citations. Previous affiliations of Olaf Ansorge include John Radcliffe Hospital.

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Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study

Elisa Majounie, +71 more
- 01 Apr 2012 - 
TL;DR: A common Mendelian genetic lesion in C9orf72 is implicated in many cases of sporadic and familial ALS and FTD, suggesting a one-off expansion occurring about 1500 years ago.
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Genetic analysis implicates APOE, SNCA and suggests lysosomal dysfunction in the etiology of Dementia with Lewy Bodies.

TL;DR: It is indicated that DLB has a unique genetic risk profile when compared with the two most common neurodegenerative diseases and that the lysosome may play an important role in the etiology of this disorder.
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Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study

Rita Guerreiro, +78 more
- 01 Jan 2018 - 
TL;DR: Despite the small sample size for a genome-wide association study, and acknowledging the potential biases from ascertaining samples from multiple locations, this study presents the most comprehensive and well powered genetic study in dementia with Lewy bodies so far.
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Genome-wide analysis of genetic correlation in dementia with Lewy bodies, Parkinson's and Alzheimer's diseases

TL;DR: Having shown that DLB shares some genetic risk with PD and AD, the amount of sharing is quantified through the application of genetic correlation estimates and it is shown that, from a purely genetic perspective, DLB is equally correlated to AD and PD.
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Analysis of neurodegenerative disease-causing genes in dementia with Lewy bodies

Tatiana Orme, +53 more
TL;DR: The rarity of previously reported pathogenic mutations in this cohort suggests that the genetic overlap of other neurodegenerative diseases with DLB is not substantial, and suggests that other genetic loci play a role in this disease.