Malú G. Tansey

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Malú Tansey
NationalityAmerican
Alma mater Stanford University
University of Texas Southwestern
Washington University in St. Louis
Known forTNF in neuroinflammation and degenerative disease
Awards2013 GIN Faculty of the Year Award Emory University, 2000 O'Leary Prize Winner, 1991 Ida M. Green Award in Physiology
Scientific career
FieldsNeuroscience
Institutions University of Florida

Malú G. Tansey is an American Physiologist and Neuroscientist as well as the Director of the Center for Translational Research in Neurodegenerative Disease at the University of Florida. Tansey holds the titles of Evelyn F. and William L. McKnight Brain Investigator and Norman Fixel Institute for Neurological Diseases Investigator. As the principal investigator of the Tansey Lab, Tansey guides a research program centered around investigating the role of neuroimmune interactions in the development and progression of neurodegenerative and neuropsychiatric disease. Tansey's work is primarily focused on exploring the cellular and molecular basis of peripheral and central inflammation in the pathology of age-related neurodegenerative diseases like Alzheimer's disease and amyotrophic lateral sclerosis.

Contents

Early life and education

In 1980, Tansey pursued her undergraduate education at Stanford University in Palo Alto, California. [1] She completed her bachelor's degree in Biological Sciences and then stayed at Stanford to complete her Master's in Biological Sciences as well. [2] After graduating in 1985, Tansey pursued her graduate studies in Physiology and Cell Cycle Regulation at the University of Texas Southwestern Medical Center. [3] Under the mentorship of James T. Stull, Tansey explored the role of myosin light chain kinase (MLCK) phosphorylation in the regulation of smooth muscle contraction. [4] Tansey found, early on in her PhD, that cellular mechanisms other than myosin light chain phosphorylation regulate contractile tension in smooth muscle cells. [5] She later found that calcium dependent phosphorylation of MLCK in smooth muscle lead to decreased calcium sensitivity of phosphorylated myosin light chains. [6] Tansey also proposed a model to understand the regulation of myosin light chain kinase phosphorylation by limited calmodulin availability. [6]

Following the completion of her graduate studies in 1992, Tansey moved to Washington University in St. Louis, Missouri, where she worked under the mentorship of Eugene M. Johnson in the Department of Molecular Pharmacology. [7] Tansey first explored the mechanisms of neuronal survival in cerebellar granule cells. [8] She and her team knew that depolarizing concentrations of potassium promoted survival, so they asked whether the downstream effects of potassium influx on survival were mediated by MAP kinase or PI-3-K. [8] They found that survival was dependent on depolarization induced PI-3-K activity. [8] Tansey then collaborated with Jeff Milbrandt's lab in the Department of Genetics at WashU to explore the GDNF family of ligands and the biology of their intracellular signalling. [7] The GDNF family of ligands (GFL) are neurotrophic factors found to be important in neuron survival, so Tansey and her colleagues probed the critical intracellular signalling component of the GFL receptor system, the receptor tyrosine kinase RET. [9] They found that in order for proper RET function and thus proper GFL signalling, RET needed to be interacting with a GPI-linked co-receptor associated with a lipid raft in order for proper functioning. [9] They further found that RET associates with members of the Src family kinases and that interaction and signalling through Src is instrumental in mediating the downstream effects of GFLs. [10]

Career and research

After completing her postdoctoral work, Tansey then moved to California to work in industry for a few years as the group leader of Chemical Genetics at Zencor Inc. in Monrovia. [7] Her work focused on developing tumor necrosis factor (TNF) inhibitors. [1] Tansey then returned to academia in 2002 and became an assistant professor of physiology at the University of Texas Southwestern. [1] At UT Southwestern, Tansey continued to study the role of the cytokine TNF in CNS signalling and disease. [7]

In 2008, Tansey was recruited to become an associate professor at Emory University in Atlanta, Georgia. Tansey became a tenured professor at Emory University, a member of the Center for Neurodegenerative Disease, and the Senior Director of Graduate Studies in Neuroscience. [11] As a Hispanic-American, Tansey worked to increase diversity and inclusion at Emory through her role as the Director of the Emory Initiative for Maximizing Student Development. [11]

In 2019, Tansey was recruited to the University of Florida to become the director of the Center for Translational Research in Neurodegenerative Disease. [12] Tansey also holds the titles of  Evelyn F, and William L McKnight Brain Investigator and Norman Fixel Institute for Neurological Diseases Investigator. [13] In addition to her leadership roles at UF, Tansey is also on the board of directors for the World Parkinson's Coalition. [7]

The Tansey Lab explores the interactions between the nervous and immune systems in the context of health and disease. [14] Tansey specifically focuses on the role of TNF in neuroinflammation and the context of Alzheimer's Disease and Parkinson's Disease. [14] Tansey also explores the roles of microglia and brain macrophages in neurological disease pathogenesis as well as how gene-environment interactions interface with chronic inflammatory states to predispose and perpetuate diseases of the central nervous system. [14]

Tumor necrosis factor signalling in disease

Tansey has been dedicated to exploring the role of TNF in disease and following the potential to inhibit its actions to ameliorate pathological inflammation in disease. [15] Since TNF had been implicated in pathology, Tansey explored a method to sequester TNF in vivo to act as an inhibitor of TNF function. [15] Tansey and her team developed a variant TNF protein that formed heterodimers with TNF in vivo rendering TNF unable to signal through TNF receptors. [15] They found that this appeared to abrogate TNF pathology in animal models. [15] Using this innovative TNF variant, Tansey and her team were able to probe the role of TNF in Alzheimer's Disease and Parkinson's Disease. [16] They found that when they blocked TNF signalling using the variant TNF technology, they were able to attenuate progressive pathology and even reduce microglial activation, which was associated with the loss of dopamine neurons in PD. [16] These findings suggested that targeting TNF might be a promising strategy to prevent the loss of dopamine neurons in PD and also prevent neuronal pathology on AD. [16]

Chronic inflammation and neurodegeneration

Tansey is a pioneer in the exploration of how chronic inflammation predisposes and perpetuates neurological disease. Contrary to previous reports, the immune system does exist in the central nervous system, and the major orchestrators of this immune response are the innate immune cells of the brain called microglia. [17] Short term activation of inflammation in the brain is present in disease, injury, or infection, and is useful in response to disease states, but if this inflammation is prolonged, it can lead to neuronal death. [17] Tansey has helped to educate the field on the concept of acute versus chronic brain inflammation, the purposes and roles of this inflammation, and its relation to chronic neurological diseases. [17] She emphasizes that microglia lie at a convergence point where stimuli can impact microglial activation and thus lead to aberrant brain inflammation and neuronal death in this way. [17] Tansey showed that the microglial GTPase RGS10 might play a protective role in a chronic inflammatory environment. [18] When RGS10 was knocked out in mice with chronic systemic inflammation, it led to overproduction of proinflammatory cytokines by microglia and death of dopaminergic neurons. [18] Since removal of RGS10 in dopaminergic neurons also made them more sensitive to the proinflammatory cytokines released by microglia, Tansey proposed RGS10 as a therapeutic target for PD. [18]

Tansey also explores the role of gene-environment interactions, or epigenetic mechanisms in neurodegenerative disease pathology and chronic inflammation. [19] She probed how diet effects immune infiltration into the brain since previous studies had showed that it might lead to compromised blood brain barrier function and increased immune cell infiltration into the CNS. [20] Conversely, her findings showed that high fat high fructose diets did not increase peripheral trafficking of immune cells into the CNS. [20] Tansey also explored the sex-specific effects of stress on neuro-immune reactivity and found that early life chronic stress led to increased neuro-immune reactivity but via different mechanisms in male versus female rats. [21]

Awards and honors

Select publications

Related Research Articles

<span class="mw-page-title-main">Glia</span> Support cells in the nervous system

Glia, also called glial cells (gliocytes) or neuroglia, are non-neuronal cells in the central nervous system and the peripheral nervous system that do not produce electrical impulses. The neuroglia make up more than one half the volume of neural tissue in our body. They maintain homeostasis, form myelin in the peripheral nervous system, and provide support and protection for neurons. In the central nervous system, glial cells include oligodendrocytes, astrocytes, ependymal cells and microglia, and in the peripheral nervous system they include Schwann cells and satellite cells.

Neurotoxicity is a form of toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the central and/or peripheral nervous system. It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant– alters the normal activity of the nervous system in such a way as to cause permanent or reversible damage to nervous tissue. This can eventually disrupt or even kill neurons, which are cells that transmit and process signals in the brain and other parts of the nervous system. Neurotoxicity can result from organ transplants, radiation treatment, certain drug therapies, recreational drug use, exposure to heavy metals, bites from certain species of venomous snakes, pesticides, certain industrial cleaning solvents, fuels and certain naturally occurring substances. Symptoms may appear immediately after exposure or be delayed. They may include limb weakness or numbness, loss of memory, vision, and/or intellect, uncontrollable obsessive and/or compulsive behaviors, delusions, headache, cognitive and behavioral problems and sexual dysfunction. Chronic mold exposure in homes can lead to neurotoxicity which may not appear for months to years of exposure. All symptoms listed above are consistent with mold mycotoxin accumulation.

<span class="mw-page-title-main">Astrogliosis</span> Increase in astrocytes in response to brain injury

Astrogliosis is an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system (CNS) trauma, infection, ischemia, stroke, autoimmune responses or neurodegenerative disease. In healthy neural tissue, astrocytes play critical roles in energy provision, regulation of blood flow, homeostasis of extracellular fluid, homeostasis of ions and transmitters, regulation of synapse function and synaptic remodeling. Astrogliosis changes the molecular expression and morphology of astrocytes, in response to infection for example, in severe cases causing glial scar formation that may inhibit axon regeneration.

<span class="mw-page-title-main">Microglia</span> Glial cell located throughout the brain and spinal cord

Microglia are a type of neuroglia located throughout the brain and spinal cord. Microglia account for about 10-15% of cells found within the brain. As the resident macrophage cells, they act as the first and main form of active immune defense in the central nervous system (CNS). Microglia originate in the yolk sac under a tightly regulated molecular process. These cells are distributed in large non-overlapping regions throughout the CNS. Microglia are key cells in overall brain maintenance—they are constantly scavenging the CNS for plaques, damaged or unnecessary neurons and synapses, and infectious agents. Since these processes must be efficient to prevent potentially fatal damage, microglia are extremely sensitive to even small pathological changes in the CNS. This sensitivity is achieved in part by the presence of unique potassium channels that respond to even small changes in extracellular potassium. Recent evidence shows that microglia are also key players in the sustainment of normal brain functions under healthy conditions. Microglia also constantly monitor neuronal functions through direct somatic contacts and exert neuroprotective effects when needed.

<span class="mw-page-title-main">Neuroprotection</span> Relative preservation of neuronal structure and/or function

Neuroprotection refers to the relative preservation of neuronal structure and/or function. In the case of an ongoing insult the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation. It is a widely explored treatment option for many central nervous system (CNS) disorders including neurodegenerative diseases, stroke, traumatic brain injury, spinal cord injury, and acute management of neurotoxin consumption. Neuroprotection aims to prevent or slow disease progression and secondary injuries by halting or at least slowing the loss of neurons. Despite differences in symptoms or injuries associated with CNS disorders, many of the mechanisms behind neurodegeneration are the same. Common mechanisms of neuronal injury include decreased delivery of oxygen and glucose to the brain, energy failure, increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation. Of these mechanisms, neuroprotective treatments often target oxidative stress and excitotoxicity—both of which are highly associated with CNS disorders. Not only can oxidative stress and excitotoxicity trigger neuron cell death but when combined they have synergistic effects that cause even more degradation than on their own. Thus limiting excitotoxicity and oxidative stress is a very important aspect of neuroprotection. Common neuroprotective treatments are glutamate antagonists and antioxidants, which aim to limit excitotoxicity and oxidative stress respectively.

<span class="mw-page-title-main">Neuroimmune system</span>

The neuroimmune system is a system of structures and processes involving the biochemical and electrophysiological interactions between the nervous system and immune system which protect neurons from pathogens. It serves to protect neurons against disease by maintaining selectively permeable barriers, mediating neuroinflammation and wound healing in damaged neurons, and mobilizing host defenses against pathogens.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes. In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar.

Neurturin (NRTN) is a protein that is encoded in humans by the NRTN gene. Neurturin belongs to the glial cell line-derived neurotrophic factor (GDNF) family of neurotrophic factors, which regulate the survival and function of neurons. Neurturin’s role as a growth factor places it in the transforming growth factor beta (TGF-beta) subfamily along with its homologs persephin, artemin, and GDNF. It shares a 42% similarity in amino acid sequence with mature GDNF. It is also considered a trophic factor and critical in the development and growth of neurons in the brain. Neurotrophic factors like neurturin have been tested in several clinical trial settings for the potential treatment of neurodegenerative diseases, specifically Parkinson's disease.

<span class="mw-page-title-main">CX3C motif chemokine receptor 1</span> Protein-coding gene in the species Homo sapiens

CX3C motif chemokine receptor 1 (CX3CR1), also known as the fractalkine receptor or G-protein coupled receptor 13 (GPR13), is a transmembrane protein of the G protein-coupled receptor 1 (GPCR1) family and the only known member of the CX3C chemokine receptor subfamily.

<span class="mw-page-title-main">Hydroxycarboxylic acid receptor 2</span> Protein-coding gene in the species Homo sapiens

Hydroxycarboxylic acid receptor 2 (HCA2), also known as GPR109A and niacin receptor 1 (NIACR1), is a protein which in humans is encoded (its formation is directed) by the HCAR2 gene and in rodents by the Hcar2 gene. The human HCAR2 gene is located on the long (i.e., "q") arm of chromosome 12 at position 24.31 (notated as 12q24.31). Like the two other hydroxycarboxylic acid receptors, HCA1 and HCA3, HCA2 is a G protein-coupled receptor (GPCR) located on the surface membrane of cells. HCA2 binds and thereby is activated by D-β-hydroxybutyric acid (hereafter termed β-hydroxybutyric acid), butyric acid, and niacin (also known as nicotinic acid). β-Hydroxybutyric and butyric acids are regarded as the endogenous agents that activate HCA2. Under normal conditions, niacin's blood levels are too low to do so: it is given as a drug in high doses in order to reach levels that activate HCA2.

<span class="mw-page-title-main">Colony stimulating factor 1 receptor</span> Protein found in humans

Colony stimulating factor 1 receptor (CSF1R), also known as macrophage colony-stimulating factor receptor (M-CSFR), and CD115, is a cell-surface protein encoded by the human CSF1R gene. CSF1R is a receptor that can be activated by two ligands: colony stimulating factor 1 (CSF-1) and interleukin-34 (IL-34). CSF1R is highly expressed in myeloid cells, and CSF1R signaling is necessary for the survival, proliferation, and differentiation of many myeloid cell types in vivo and in vitro. CSF1R signaling is involved in many diseases and is targeted in therapies for cancer, neurodegeneration, and inflammatory bone diseases.

<span class="mw-page-title-main">RIPK1</span> Enzyme found in humans

Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) functions in a variety of cellular pathways related to both cell survival and death. In terms of cell death, RIPK1 plays a role in apoptosis and necroptosis. Some of the cell survival pathways RIPK1 participates in include NF-κB, Akt, and JNK.

<span class="mw-page-title-main">TREM2</span> Protein-coding gene in the species Homo sapiens

Triggering receptor expressed on myeloid cells 2(TREM2) is a protein that in humans is encoded by the TREM2 gene. TREM2 is expressed on macrophages, immature monocyte-derived dendritic cells, osteoclasts, and microglia, which are immune cells in the central nervous system. In the liver, TREM2 is expressed by several cell types, including macrophages, that respond to injury. In the intestine, TREM2 is expressed by myeloid-derived dendritic cells and macrophage. TREM2 is overexpressed in many tumor types and has anti-inflammatory activities. It might therefore be a good therapeutic target.

<span class="mw-page-title-main">Quinolinic acid</span> Dicarboxylic acid with pyridine backbone

Quinolinic acid, also known as pyridine-2,3-dicarboxylic acid, is a dicarboxylic acid with a pyridine backbone. It is a colorless solid. It is the biosynthetic precursor to niacin.

Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. In the central nervous system (CNS), including the brain and spinal cord, microglia are the resident innate immune cells that are activated in response to these cues. The CNS is typically an immunologically privileged site because peripheral immune cells are generally blocked by the blood–brain barrier (BBB), a specialized structure composed of astrocytes and endothelial cells. However, circulating peripheral immune cells may surpass a compromised BBB and encounter neurons and glial cells expressing major histocompatibility complex molecules, perpetuating the immune response. Although the response is initiated to protect the central nervous system from the infectious agent, the effect may be toxic and widespread inflammation as well as further migration of leukocytes through the blood–brain barrier may occur.

<span class="mw-page-title-main">Pathophysiology of Parkinson's disease</span> Medical condition

The pathophysiology of Parkinson's disease is death of dopaminergic neurons as a result of changes in biological activity in the brain with respect to Parkinson's disease (PD). There are several proposed mechanisms for neuronal death in PD; however, not all of them are well understood. Five proposed major mechanisms for neuronal death in Parkinson's Disease include protein aggregation in Lewy bodies, disruption of autophagy, changes in cell metabolism or mitochondrial function, neuroinflammation, and blood–brain barrier (BBB) breakdown resulting in vascular leakiness.

Microglia are the primary immune cells of the central nervous system, similar to peripheral macrophages. They respond to pathogens and injury by changing morphology and migrating to the site of infection/injury, where they destroy pathogens and remove damaged cells.

<span class="mw-page-title-main">Inflammaging</span> Chronic low-grade inflammation that develops with advanced age

Inflammaging is a chronic, sterile, low-grade inflammation that develops with advanced age, in the absence of overt infection, and may contribute to clinical manifestations of other age-related pathologies. Inflammaging is thought to be caused by a loss of control over systemic inflammation resulting in chronic overstimulation of the innate immune system. Inflammaging is a significant risk factor in mortality and morbidity in aged individuals.

<span class="mw-page-title-main">Katerina Akassoglou</span> Greek neuroimmunologist

Katerina Akassoglou is a neuroimmunologist who is a Senior Investigator and Director of In Vivo Imaging Research at the Gladstone Institutes. Akassoglou holds faculty positions as a Professor of Neurology at the University of California, San Francisco. Akassoglou has pioneered investigations of blood-brain barrier integrity and development of neurological diseases. She found that compromised blood-brain barrier integrity leads to fibrinogen leakage into the brain inducing neurodegeneration. Akassoglou is internationally recognized for her scientific discoveries.

References

  1. 1 2 3 "Malú Tansey". www.journals.elsevier.com. Retrieved 2020-05-22.
  2. ↑ "Tansey Lab Members". ctrnd.med.ufl.edu. Retrieved 2020-05-22.
  3. ↑ "Malú G. Tansey, Ph.D." www.physiology.emory.edu. Retrieved 2020-05-22.
  4. ↑ "Malu G. Tansey - Google Scholar Citations". scholar.google.com. Retrieved 2020-05-22.
  5. ↑ Tansey, M.G.; Hori, M.; Karaki, H.; Kamm, K.E.; Stull, J.T. (17 September 1990). "Okadaic acid uncouples myosin light chain phosphorylation and tension in smooth muscle". FEBS Letters. 270 (1–2): 219–221. doi: 10.1016/0014-5793(90)81272-P . PMID   2171992. S2CID   5857606.
  6. 1 2 Tansey, M. G.; Word, R. A.; Hidaka, H.; Singer, H. A.; Schworer, C. M.; Kamm, K. E.; Stull, J. T. (25 June 1992). "Phosphorylation of myosin light chain kinase by the multifunctional calmodulin-dependent protein kinase II in smooth muscle cells". Journal of Biological Chemistry. 267 (18): 12511–12516. doi: 10.1016/S0021-9258(18)42307-1 . PMID   1319999.
  7. 1 2 3 4 5 "Board of Directors - World Parkinson Coalition". www.worldpdcoalition.org. Retrieved 2020-05-22.
  8. 1 2 3 Miller, Timothy M.; Tansey, Malú G.; Johnson, Eugene M.; Creedon, Douglas J. (11 April 1997). "Inhibition of Phosphatidylinositol 3-Kinase Activity Blocks Depolarization- and Insulin-like Growth Factor I-mediated Survival of Cerebellar Granule Cells". Journal of Biological Chemistry. 272 (15): 9847–9853. doi: 10.1074/jbc.272.15.9847 . PMID   9092520. S2CID   19330474.
  9. 1 2 Tansey, Malú G.; Baloh, Robert H.; Milbrandt, Jeffrey; Johnson, Eugene M. (March 2000). "GFRα-Mediated Localization of RET to Lipid Rafts Is Required for Effective Downstream Signaling, Differentiation, and Neuronal Survival". Neuron. 25 (3): 611–623. doi: 10.1016/S0896-6273(00)81064-8 . PMID   10774729. S2CID   11467713.
  10. ↑ Encinas, Mario; Tansey, Malú G.; Tsui-Pierchala, Brian A.; Comella, Joan X.; Milbrandt, Jeffrey; Johnson, Eugene M. (1 March 2001). "c-Src Is Required for Glial Cell Line-Derived Neurotrophic Factor (GDNF) Family Ligand-Mediated Neuronal Survival via a Phosphatidylinositol-3 Kinase (PI-3K)-Dependent Pathway". The Journal of Neuroscience. 21 (5): 1464–1472. doi:10.1523/JNEUROSCI.21-05-01464.2001. PMC   6762937 . PMID   11222636.
  11. 1 2 "McKnight Brain Institute Neuromedicine Scholars" (PDF). Retrieved May 21, 2020.
  12. ↑ "Renowned neuroscientists to join UF Health, propel discovery of treatments for neurological diseases". McKnight Brain Institute, University of Florida. March 18, 2019. Retrieved 2020-05-22.
  13. ↑ "Dr. Tansey Named the Principal Investigator of a new Parkinson's Foundation Research Center of Excellence Award". Center for Translational Research in Neurodegenerative Disease. July 30, 2019. Retrieved 2020-05-22.
  14. 1 2 3 "Tansey Lab Research". ctrnd.med.ufl.edu. Retrieved 2020-05-22.
  15. 1 2 3 4 Steed, Paul M.; Tansey, Malú G.; Zalevsky, Jonathan; Zhukovsky, Eugene A.; Desjarlais, John R.; Szymkowski, David E.; Abbott, Christina; Carmichael, David; Chan, Cheryl; Cherry, Lisa; Cheung, Peter; Chirino, Arthur J.; Chung, Hyo H.; Doberstein, Stephen K.; Eivazi, Araz; Filikov, Anton V.; Gao, Sarah X.; Hubert, René S.; Hwang, Marian; Hyun, Linus; Kashi, Sandhya; Kim, Alice; Kim, Esther; Kung, James; Martinez, Sabrina P.; Muchhal, Umesh S.; Nguyen, Duc-Hanh T.; O'Brien, Christopher; O'Keefe, Donald; Singer, Karen; Vafa, Omid; Vielmetter, Jost; Yoder, Sean C.; Dahiyat, Bassil I. (26 September 2003). "Inactivation of TNF Signaling by Rationally Designed Dominant-Negative TNF Variants". Science. 301 (5641): 1895–1898. Bibcode:2003Sci...301.1895S. doi:10.1126/science.1081297. PMID   14512626. S2CID   33782456.
  16. 1 2 3 Tansey, Malu G; McCoy, Melissa K; Frank-Cannon, Tamy; McAlpine, Fiona E; Botterman, Barry R; Tansey, Keith E (6 March 2006). "The role of TNF in in vitro and in vivo models of neurodegeneration". The FASEB Journal. 20 (4): A505. doi: 10.1096/fasebj.20.4.A505-b . S2CID   227192984.
  17. 1 2 3 4 Frank-Cannon, Tamy C; Alto, Laura T; McAlpine, Fiona E; Tansey, Malú G (2009). "Does neuroinflammation fan the flame in neurodegenerative diseases?". Molecular Neurodegeneration. 4 (1): 47. doi: 10.1186/1750-1326-4-47 . PMC   2784760 . PMID   19917131.
  18. 1 2 3 Lee, Jae Kyung; McCoy, Melissa K; Harms, Ashley S; Ruhn, Kelly A; Gold, Stephen J; Tansey, Malu G (1 March 2008). "Regulator of G-protein signaling (RGS10) regulates microglial response to chronic inflammatory stimuli and impacts dopaminergic neuron survival". The FASEB Journal. 22 (1_supplement): 1072.5. doi: 10.1096/fasebj.22.1_supplement.1072.5 . S2CID   224080607.
  19. ↑ Tansey, Malú G.; McCoy, Melissa K.; Frank-Cannon, Tamy C. (November 2007). "Neuroinflammatory mechanisms in Parkinson's disease: Potential environmental triggers, pathways, and targets for early therapeutic intervention". Experimental Neurology. 208 (1): 1–25. doi:10.1016/j.expneurol.2007.07.004. PMC   3707134 . PMID   17720159.
  20. 1 2 Sniffen, Lindsey J.; Eidson, Lori N.; Herrick, Mary K.; MacPherson, Kathryn P.; de Sousa Rodrigues, Maria E.; Tansey, Malu G. (1 April 2018). "Effect of High Fat High Fructose Diet on Peripheral Immune Cell Trafficking into the Brain in CCR2 Mouse Model". The FASEB Journal. 32 (1_supplement): 740.10. doi: 10.1096/fasebj.2018.32.1_supplement.740.10 . S2CID   222602016.
  21. ↑ Bekhbat, M.; Mukhara, D.; Dozmorov, M. J.; Stansfield, J. C.; Benusa, S. D.; Rowson, S. A.; Kelly, S. D.; Tharp, G. K.; Tansey, M. G.; Neigh, G. N. (1 February 2019). "Abstract # 3111 Chronic adolescent stress differentially sensitizes neuro-immune reactivity in male and female rats". Brain, Behavior, and Immunity. 76: e20. doi:10.1016/j.bbi.2018.11.235. S2CID   71716295.
  22. ↑ "Women who inspire researchers making their mark" . Retrieved May 21, 2020.
  23. ↑ "2012-2013 Honors and Awards| GDBBS | Emory University". biomed.emory.edu. Retrieved 2020-05-22.
  24. ↑ "O'Leary Prize recipients | Office of Neuroscience Research | Washington University in St. Louis". neuroscienceresearch.wustl.edu. Retrieved 2020-05-22.
  25. ↑ "Previous Ida M. Green Award Recipients". www.utsouthwestern.edu. Retrieved 2020-05-22.
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