scispace - formally typeset
J

Jason L. Eriksen

Researcher at University of Houston

Publications -  79
Citations -  13566

Jason L. Eriksen is an academic researcher from University of Houston. The author has contributed to research in topics: Alzheimer's disease & Frontotemporal lobar degeneration. The author has an hindex of 30, co-authored 77 publications receiving 12656 citations. Previous affiliations of Jason L. Eriksen include Mayo Clinic & University of Houston System.

Papers
More filters
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17

Matt Baker, +26 more
- 24 Aug 2006 - 
TL;DR: It is demonstrated that in multiple FTD families with significant evidence for linkage to the same region on chromosome 17q21, FTD is caused by mutations in progranulin (PGRN) that are likely to create null alleles and identified mutations in PGRN as a cause of neurodegenerative disease.
Journal ArticleDOI

A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity

Sascha Weggen, +13 more
- 08 Nov 2001 - 
TL;DR: It is reported that the NSAIDs ibuprofen, indomethacin and sulindac sulphide preferentially decrease the highly amyloidogenic Aβ42 peptide (the 42-residue isoform of the amyloids-β peptide) produced from a variety of cultured cells by as much as 80%.
Journal ArticleDOI

NSAIDs and enantiomers of flurbiprofen target γ-secretase and lower Aβ42 in vivo

Jason L. Eriksen, +10 more
- 01 Aug 2003 - 
TL;DR: R-flurbiprofen reduces Aβ42 levels by targeting γ-secretase and has reduced side effects related to inhibition of cyclooxygenase (COX), it is an excellent candidate for clinical testing as an A β42 lowering agent.
Journal ArticleDOI

Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice

Eileen McGowan, +19 more
- 21 Jul 2005 - 
TL;DR: Transgenic models that express Abeta1-40 or Abeta2-42 in the absence of human amyloid beta protein precursor (APP) overexpression establish that Abeta 1-42 is essential for amyloids deposition in the parenchyma and also in vessels.