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| First Name: | Douglas | | Last Name: | Feinstein | | Title: | Dr. | | Advanced Degrees: | PhD | | Affiliation: | Univ of Illinois | | Department: | Anesthesiology | | Street Address 1: | 835 S Wolcott St | | Street Address 2: | mc513 room 720 | | City: | chicago | | State/Province: | IL | | Zip/Postal Code: | 60612 | Country/Territory: | U.S.A. | | Phone: | 312-355-1665 | | Fax: | 815-333-0449 | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 13 December 2010]
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View all comments by Douglas Feinstein
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Oxidative Stress, Molecular and Cell biology, Clinical trials, Animal Models, Bioinformatics/Statistics, Proteomics, A-beta PP/A-beta, Neurobiology, Signal transduction, Neuroimmunology, ppars, DNA microarrays
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1977 BS, Mass Inst Technology, Boston, MA
1984 PhD, Johns Hopkins Univ., Baltimore, MB
1986 Postdoc, Res Inst Scripps Clinic, San Diego, CA
1989 Univ of Uppsala, Sweden
1990 Univ of Lausanne, Switzerland
1991 Asst Prof, Cornell Univ Med. College, NY, NY
1996 Assoc. Prof, CUMC, NY, NY
1997 Assoc Prof, Dept of Anesthesiogloy, Univ of Illinois, Chicago
2002 Res. Biologist, VA West Side, Chicago, IL
Research Summmary:
Regulation of neuro-inflammatory responses in astrocytes, and the expression of the inducible form of Nitric Oxide Synthase.
Regulation of neuroinflammatory responses in glia and neurons, using cell culture and animal models of AD and MS.
He and Dr. Galea identified iNOS expression in brain glial cells, and that noradrenaline restricts neuro-inflammation in brain (1), which may be relevant to AD where noradrenergic neurons are lost (2).
With Dr. Michael Heneka, they characterized anti-inflammatory actions of PPARg agonists in neural cultures, and that these drugs prevent the clinical symptoms of EAE, the animal model of MS (3).
Papers: 63
Editorial Boards: JNeuroimmunology, J. Neurochemistry, Brain Research
Funding: NIH, VA, and private agencies.
1. Feinstein D, Heneka M, Gavrilyuk V, Russo C, Weinberg G, Galea E. (2002) Noradrenergic regulation of inflammatory gene expression in brain. Neurochem Int. 41:357.
2. Heneka MT, Galea E, Gavriluyk V, Dumitrescu-Ozimek L, Daeschner J, O'Banion MK, Weinberg G, Klockgether T, Feinstein DL. (2002) Noradrenergic depletion potentiates b-amyloid induced inflammation in frontal cortex: Implications for Alzheimer's disease J. Neuroscience, 22(7):2434-42.
3. Feinstein DL, Galea E, Gavrilyuk V, Brosnan CF, Whitacre CC, Dumitrescu-Ozimek L, Landreth GE, Pershadsingh HA, Weinberg G, Heneka MT. (2002) Prevention and treatment of experimental autoimmune encephalomyelitis by pioglitazone, a PPARg agonist Annals Neurology, 51(6):694-708.
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1. Polak, PE, Kalinin, S., and Feinstein DL. (2011) “Damage to the Locus coeruleus occurs in MS and EAE” Brain, in press
2 Simonini, MV; Polak PE; Sharp, A.; McGuire, S.; Galea, E.; and Feinstein, DL (2010) Increasing Central Noradrenaline Reduces EAE Severity, J Neuroimmune Pharmacol. 5(2):252-9. Epub 2009 Dec 4.
3 Kalinin, S; Richardson, JC, and Feinstein, DL (2009) “A PPARdelta Agonist Reduces Amyloid Burden and Brain Inflammation in Transgenic Mouse Model of Alzheimer's Disease.” Current Alzheimer’s Research, 6(5):431-7.
4 C.C. Kaiser; D.D. Skias; D.K. Shukla; G.T. Stebbins; D.R. Jeffery; D. Stefoski; G. Katsamakis; D.L. Feinstein (2009) A placebo-controlled randomized trial of Pioglitazone as add-on in Relapsing Remitting MS Patients, J. Neuroimmunology, 211(1-2):124-30
5 Kalinin S, Gavrilyuk V, Polak PE, Heneka MT, and Feinstein DL (2007) “Noradrenaline deficiency in brain increases -amyloid plaque burden in an animal model of Alzheimer’s disease” Neurobio Aging, 28(8):1206-14
6 Feinstein D.L, Spagnolo A., Akar C., Weinberg G., Murphy P., Gavrilyuk V. and Dello Russo C. (2005)“Receptor-independent actions of PPAR thiazolidinedione agonists: Is mitochondrial function the key?” Biochem. Pharmacology, 70(2):177-88
7 Heneka MT, Galea E, Gavriluyk V, Dumitrescu-Ozimek L, Daeschner J, O'Banion MK, Weinberg G, Klockgether T, Feinstein DL. (2002) “Noradrenergic depletion potentiates b-amyloid induced inflammation in frontal cortex: Implications for Alzheimer’s disease” J. Neuroscience, 22(7):2434-42.
8 Feinstein DL, Galea E, Gavrilyuk V, Brosnan CF, Whitacre CC, Dumitrescu-Ozimek L, Landreth GE, Pershadsingh HA, Weinberg G, Heneka MT. (2002) “Prevention and treatment of experimental autoimmune encephalomyelitis by pioglitazone, a PPAR-g agonist” Annals Neurology, 51(6):694-708. |
Identification of non-genomic (i.e. environmental and epigenetic) factors which initiate cascades leading to increased Ab production. |
Wyss-Coray T, Mucke L.
Inflammation in neurodegenerative disease--a double-edged sword.
Neuron. 2002 Aug 1;35(3):419-32. Review.
Almeida A, Almeida J, Bolanos JP, Moncada S. Different responses of astrocytes and neurons to nitric oxide: the role of glycolytically generated ATP in astrocyte protection.
Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15294-9.
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Large scale differential proteomic screening of TgAPP vs WT mice, with and without therapeutic treatments |
LC dysfunction is a major contributor to AD pathogenesis |
LC specific conditional knockouts |
Compensatory increases in surviving neurons |
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