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Matthew J. Huentelman

Researcher at Translational Genomics Research Institute

Publications -  77
Citations -  15262

Matthew J. Huentelman is an academic researcher from Translational Genomics Research Institute. The author has contributed to research in topics: Medicine & Genome-wide association study. The author has an hindex of 34, co-authored 51 publications receiving 13225 citations. Previous affiliations of Matthew J. Huentelman include University of Florida & Ohio University.

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Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease

Jean-Charles Lambert, +215 more
- 01 Dec 2013 - 
TL;DR: In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.
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Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease.

Adam C. Naj, +156 more
- 01 May 2011 - 
TL;DR: The Alzheimer Disease Genetics Consortium performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1), two replication stages (stages 2 and 3), and both joint analysis and meta-analysis approaches were used.
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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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Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

Rebecca Sims, +487 more
- 01 Sep 2017 - 
TL;DR: Three new genome-wide significant nonsynonymous variants associated with Alzheimer's disease are observed, providing additional evidence that the microglia-mediated innate immune response contributes directly to the development of Alzheimer's Disease.
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Recessive Symptomatic Focal Epilepsy and Mutant Contactin-Associated Protein-like 2

TL;DR: A homozygous mutation of CNTNAP2 is reported in Old Order Amish children with cortical dysplasia, focal epilepsy, relative macrocephaly, and diminished deep-tendon reflexes, with evidence of abnormalities of neuronal migration and structure, widespread astrogliosis, and reduced expression of CASPR2.