Diana I Lurie



Personal Summary

After completing undergraduate work in Biopsychology at Wesleyan University in Middletown, CT, Diana Lurie received her Ph.D. in Neuroscience from the University of Pennsylvania in 1989. Following a postdoctoral fellowship at the University of Washington, she moved to The University of Montana as an Assistant Professor in 1995 and is currently a Full Professor.  Dr. Lurie is also a certified Ayurvedic Practioner and the Editor-in-Chief for the Ayurveda Journal of Health.


1980-84  B.A. Biopsychology   Wesleyan University

1984-89  Ph.D.Neuroscience     University of Pennsylvania

1989-1990 Postdoctoral Fellowship,  University of Pennsylvania

1990-1995  Postdoctoral Fellowship, University of Washington

Courses Taught

Phar 341  Physiolgoical Systems

Phar 362  Pharmaceutical Sciences Lab

Phar 371, 372  Integrated studies

Phar 110  Use and Abuse of Drugs

Phar 395.02  Native American Medicine

Phar 324  Medicinal Plants

Phar 391.01  Overview of Ayurvedic Medicine

BMED 662  Neuroscience 2

Research Interests

Research in the Lurie laboratory focuses on the CNS response to injury and disease, with a particular emphasis on the glial response to injury.  Previous work in the Lurie laboratory has focused on the role that tyrosine phosphorylation plays in the signal transduction events that occur following damage to the nervous system, particularly in stroke.  In addition, our group has also examined the ways in which low levels of lead exposure modulate the development of  sensory systems in the brainstem, with a focus on the developing auditory system.  

Recently, we have turned our attention to the role that inflammatory processes play in CNS dysfunction such as stroke, andneurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease.  Interestingly, inflammation in the CNS is now thought to play a role in diseases such as depression, anxiety, and schizophrenia.  Inflammation in the CNS is modulated by microglial cells; the immune cells of the nervous system.  Following injury and during neurodegeneration, microglia become activated and release a variety of cytokines and factors that contribute to inflammatory cascades within the CNS.   Increases in these proinflammatory cytokines are associated with neurodegeneration as well as depression and schizophrenia.  It is thought that inhibiting the release of proinflammatorycytokines from activated microglia might help to ameliorate the neuronal damage and dysfunction that occurs during these diseases processes. 

Our laboratory is currently examining a variety of natural products for their ability to inhibit the release of proinflammatory cytokines from activated microglia in vitro.  We are focusing on the Ayurvedic herbs  Bacopa Monnieri, Gotu Kola, and Ashwagandha to determine which compounds have the ability to limit proinflammatory cytokine release from microglia. We are also examining the ability of curcumin, the active compound in turmeric, to limit the neurodegenerative processes that occur during Alzheimer’s disease in a collaborative project with the Coffin laboratory (BMED).   Techniques employed in the laboratory include non-radioactive enzyme activity assays, ELISA, cell proliferation and cell death assays, cell culture, tissue histology and immunocytochemistry, and image analysis.

The Lurie lab maintains active collaborations with other research groups at the University of Washington, the University of Kansas Medical Center, and Laila Pharma, Vijayawada India. Dr. Lurie is also a certified Ayurvedic Practioner and the Editor-in-Chief for theAyurveda Journal of Health.


The role of the Ayurvedic herb Bacopa monnieri in neuroinflammation

Natural product therapeutics for Alzheimer's Disease

Field of Study


Complementary and Alternative Medicine


Natural Product Therapeutics

Selected Publications

Book Chapters

Lurie DI and Coffin, JD (2015) The role of bacopa monnieri in inflammatory and neurodegenerative diseases.  In Occurrences, Structure, Biosynthesis, and Health Benefits Based on Their Evidences of Medicinal Phytochemicals in Vegetables and Fruits.  Ed. Noboru Motohashi.  Volume 3. Nova Science Publishers, NY, USA. In press.

Prins JM, Wang Y, Lurie DI (2013) Quantitative proteomic approaches for environmental toxicology.  In Recent Advances in Proteomics Research.  Ed. Ming Li, Nova Science Publishers, NY.  Chapter 9, pgs 219-238.

Lurie DI (2013)  A scientific examination of western dietary practices as they relate to food practices in Ayurveda.  In Ayurvedic Science of Food and Nutrition.  Ed. Sanjeev Rastogi, Springer, USA.  Chapter 11 pp 139-160.

Selected Publications

Park S, Nevin AB, Cardozo-Pelaez F, Lurie DI (2016)  Pb exposure extends the time period for postnatal transient uptake of 5-HT by murine LSO neurons.  Neurotoxicology. 2016 Oct 19;57:258-269. doi: 10.1016/j.neuro.2016.10.010. [Epub ahead of print] PMID: 27771255

Nemetchek MD, Stierle AA, Stierle Stierle DB, Lurie DI (2016).  The Ayurvedic plant Bacopa Monnieri inhibits inflammatory pathways in the brain.    Journal of Ethnopharmacology.  2016 Jul 26. pii: S0378-8741(16)30495-0. doi: 10.1016/j.jep.2016.07.073. [Epub ahead of print] PMID: 27473605

Prins JM, Brooks D, Thompson C, Lurie DI (2010) Chronic low-level Pb exposure during development decreases the expression of the voltage dependent anion channel in auditory neurons of the brainstem.  Neurotoxicology 31(6):662-673.

Prins JM, Park S, Lurie DI (2010) Decreased expression of the voltage-dependent anion channel in differentiated PC-12 and SH-SY5Ycells following Low-level Pb exposure.  Toxicological Sciences 113(1): 169-176.

Tyler T and Lurie DI (2009)  Chronic low-level lead exposure affects the monoaminergic system in the mouse superior olivary complex.  J. Comp. Neurol.  513(542-58).

Harris JA, Iguchi F, Seidl AH, Lurie DI, Rubel EW (2008)  Afferent deprivation elicits a transcriptional response associated with neuronal survival after a critical period in the mouse cochlear nucleus.  J. Neurosci.  28(43):10990-11002.

Jones LG, Prins J, Park S, Walton JP, Leubke AE, Lurie DI (2008)  Lead exposure during development results in increasedneurofilament phosphorylation, neuritic beading, and temporal processing deficits within the murine auditory brainstem.  Journal of Comparative Neurology, 506(6): 1003-1017.

Beamer CA, Brooks DM, Lurie DI (2006)  Motheaten (me/me) mice deficient in SHP-1 are less susceptible to focal cerebral ischemia.  J.Neurosci. Res 83(7):1220-1230.

Zhao J, Brooks D, Lurie DI (2006) Lipopolysaccharide-activated  SHP-1 deficient motheaten microglia release increased nitric oxide,TNF-aand IL-1b,  Glia 53(3):304-312.

Zhao and Lurie (2004)  Loss of SHP-1 phosphatase selectively alters cytokine expression in the mouse hindbrain following cochlear ablation.   Cytokine, 28:1-9.

Zhao and Lurie (2004)  Cochlear Ablation in mice lacking SHP-1 results in an extended period of cell death in anteroventral cochlear nucleus neurons.  Hearing Res. 189:63-75.


Affiliate Professor, University of Washington, Deptartment of Otolaryngology-HNS

Society for Neuroscience

National Ayurvedic Medica Association (NAMA)

Association of Ayurvedic Professionals of North America (AAPNA)

American Botanical Council

Honors / Awards

2010                Inducted into Phi Kappa Phi as an honorary faculty member.