scispace - formally typeset
B

Bruno A. Benitez

Researcher at Washington University in St. Louis

Publications -  86
Citations -  5009

Bruno A. Benitez is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Genome-wide association study & Biology. The author has an hindex of 26, co-authored 68 publications receiving 3106 citations. Previous affiliations of Bruno A. Benitez include National University of Colombia & University of Washington.

Papers
More filters
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal ArticleDOI

Rare coding variants in the phospholipase D3 gene confer risk for Alzheimer’s disease

Carlos Cruchaga, +79 more
- 23 Jan 2014 - 
TL;DR: The genetic and functional data indicate that carriers of PLD3 coding variants have a twofold increased risk for LOAD and thatPLD3 influences APP processing, and provides an example of how densely affected families may help to identify rare variants with large effects on risk for disease or other complex traits.
Journal ArticleDOI

Coding variants in TREM2 increase risk for Alzheimer's disease

TL;DR: Gene-based tests demonstrate variants in TREM2 are genome-wide significantly associated with AD, and gel electrophoresis analysis confirms that at least three T REM2 transcripts are expressed in human brains, including one encoding a soluble form of TREM1.
Journal ArticleDOI

TREM2 variant p.R47H as a risk factor for sporadic amyotrophic lateral sclerosis

TL;DR: This study demonstrates that the TREM2 p.R47H variant was more common in patients with ALS than in the controls and is therefore a significant risk factor for ALS, and highlights the T REM2 signaling pathway as a therapeutic target in ALS and other neurodegenerative diseases.