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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Linda
Last Name:Van Eldik
Title:Director, Sanders-Brown Center on Aging; Vernon Smith Endowed Professor > in Alzheimer Research; Professor, Dept. Anatomy and Neurobiology
Advanced Degrees:Ph.D.
Affiliation:University of Kentucky
Department:Department of Anatomy and Neurobiology
Street Address 1:101 Sanders-Brown Bldg.
Street Address 2:800 S. Limestone St.
City:Lexington
State/Province:KY
Zip/Postal Code:40507
Country/Territory:U.S.A.
Phone:859-323-6040
Email Address: 
Disclosure:
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View all comments by Linda Van Eldik
Clinical Interests:
Alzheimer Disease
Research Focus:
Neuroinflammation, drug discovery, Molecular and Cell biology, Proteomics, A-beta PP/A-beta, Neurobiology, Signal transduction
Work Sector(s):
University
Web Sites:
Professional: http://ddp.northwestern.edu
Researcher Bio
PhD, 1977, Duke University
Postdoctoral 1978-81, Rockefeller University
Asst, Assoc, Full Professor, 1981-94, Vanderbilt University
Full Professor, 1994-present, Northwestern Univ
Associate Director of Northwestern Alzheimer's Disease Center
Top Papers
Sheng JG, Ito K, Skinner RD, Mrak RE, Rovnaghi CR, Van Eldik LJ and Griffin WST (1996) In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis. Neurobiology of Aging 17:761-766.

Hu J, Akama KT, Krafft GA, Chromy BA and Van Eldik LJ (1998) Amyloid beta peptide activates cultured astrocytes: morphological alterations, cytokine induction and nitric oxide release. Brain Research 785:195-206.

Akama KT, Albanese C, Pestell RG and Van Eldik LJ (1998) Amyloid beta-peptide stimulates nitric oxide production in astrocytes through an NFkB-dependent mechanism. Proc Natl Acad Sci USA 95:5795-5800.

Petrova TV, Akama KT and Van Eldik LJ (1999) Cyclopentenone prostaglandins suppress activation of microglia: downregulation of inducible nitric oxide synthase by 15-deoxy-*12,14 prostaglandin J2. Proc Natl Acad Sci USA 96:4668-4673.

Petrova TV, Akama KT and Van Eldik LJ (1999) Selective modulation of BV-2 microglial activation by prostaglandin E2: differential effects on endotoxin-stimulated cytokine induction. J Biol Chem 274:28823-28827.

Hu J and Van Eldik LJ (1999) Glial-derived proteins activate cultured astrocytes and enhance b amyloid- induced astrocyte activation. Brain Res 842:46-54.

Akama KT and Van Eldik LJ (2000) beta-Amyloid stimulation of inducible nitric oxide synthase in astrocytes is interleukin-1beta- and tumor necrosis factor-alpha (TNFa)-dependent, and involves a TNFa receptor-associated factor- and NFkB-inducing kinase-dependent signaling mechanism. J Biol Chem 275: 7918-7924.

LaDu MJ, Shah JA, Reardon K, Getz GS, Bu G, Hu J, Guo L and Van Eldik LJ (2000) Apolipoprotein E receptors mediate the effects of beta-amyloid on primary astrocyte cultures. J Biol Chem 275:33974-33980.

Watterson DM, Mirzoeva S, Guo L, Whyte A, Bourguignon J-J, Hibert M, Haiech J and Van Eldik LJ (2001) Ligand modulation of glial activation: cell permeable, small molecule inhibitors of serine-threonine protein kinases can block induction of interleukin-1b and nitric oxide synthase II. Neurochem Intl 39: 459-468.

Mirzoeva S, Sawkar A, Zasadzki M, Guo L, Velentza A, Dunlap V, Bourguignon J-J, Ramstrom H, Haiech J, Van Eldik LJ and Watterson DM (2002) Discovery of a 6-amino-3-phenylpyridazine derivative as a new synthetic anti-neuroinflammatory compound. J Med Chem 45: 563-566.
What is the greatest void to date in our knowledge of Alzheimer's Disease?
The quantitative contribution of each of the large number of contributing factors to AD progression.

If resources were not limited, what research projects would you pursue?
Drug discovery
What is your leading hypothesis?
Selective anti-neuroinflammatory compounds that block the detrimental signal transduction responses of chronically activated glial cells will be useful to slow progression of pathology in AD.
What piece of missing evidence would help prove it?
We are testing this hypothesis now by developing these kinds of selective compounds, and testing them in relevant cell-based and animal models.
What is your fallback position?
It's working so far. We may have to target different pathways if the particular compounds we test do not work like we anticipate.

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