Albert A. Davis
Washington University in St. Louis
25 Papers
30 Citations
Albert A. Davis is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Medicine & Genome-wide association study. The author has an hindex of 10, co-authored 25 publications.
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Papers
Apolipoprotein E and Alzheimer's disease: the influence of apolipoprotein E on amyloid-β and other amyloidogenic proteins
TL;DR: The role of apoE on the biophysical properties and metabolism of the Aβ peptide, the principal component of amyloid plaques and cerebral amyloids angiopathy, is discussed and the discussion is extended to the potential role of APOE on other amyloidalogenic proteins found in AD, and also a number of diverse neurodegenerative diseases.
190
APOE genotype regulates pathology and disease progression in synucleinopathy
Albert A. Davis,Casey E. Inman,Zachary M. Wargel,Umber Dube,Brittany M. Freeberg,Alexander Galluppi,Jessica N. Haines,Dhruva Dhavale,Rebecca L. Miller,Fahim A. Choudhury,Patrick Sullivan,Carlos Cruchaga,Joel S. Perlmutter,Jason D. Ulrich,Bruno A. Benitez,Paul T. Kotzbauer,David M. Holtzman +16 more
TL;DR: It is demonstrated that APOE genotype directly regulates α-synuclein pathology independent of its established effects on Aβ and tau, corroborate the finding that APoe ε4 exacerbates pathology, and suggest thatAPOE ε2 may protect against αSyn aggregation and neurodegeneration in synucleinopathies.
152
Resequencing analysis of five Mendelian genes and the top genes from genome-wide association studies in Parkinson’s Disease
Bruno A. Benitez,Albert A. Davis,Sheng Chih Jin,Laura Ibanez,Sara Ortega-Cubero,Pau Pastor,Pau Pastor,Jae-Young Choi,Breanna Cooper,Joel S. Perlmutter,Carlos Cruchaga +10 more
TL;DR: The data suggest that the impact of additional untested coding variants in the GBA and LRRK2 genes is higher than previously estimated and provide compelling evidence of the existence of additionalUntested variants inThe primary Mendelian and PD GWAS genes that contribute to the genetic etiology of sporadic PD.
TDP-43 dysfunction results in R-loop accumulation and DNA replication defects
Matthew D. Wood,Matthew D. Wood,Annabel Quinet,Yea-Lih Lin,Albert A. Davis,Philippe Pasero,Yuna M. Ayala,Alessandro Vindigni,Alessandro Vindigni +8 more
TL;DR: It is shown that loss of TDP-43 increases R-loop formation in a transcription-dependent manner and results in DNA replication stress, and it is proposed that the increased R- loop formation and genomic instability associated with T DP-43 loss are linked to the pathogenesis of TPD-43 proteinopathies.
56
Overlapping genetic architecture between Parkinson disease and melanoma
Umber Dube,Laura Ibanez,John P. Budde,Bruno A. Benitez,Albert A. Davis,Oscar Harari,Mark M. Iles,Matthew Law,Kevin M. Brown,Carlos Cruchaga +9 more
TL;DR: Polygenic, linkage disequilibrium-informed methods are applied to the largest available case–control, genome-wide association study summary statistic data for melanoma and PD to demonstrate specific, shared genetic architecture between PD and melanoma that manifests at the level of gene expression.