Staci Bilbo is an American neuroimmunologist and The Haley Family Professor of Psychology and Neuroscience at Duke University. Bilbo also holds a position as a research affiliate at Massachusetts General Hospital overseeing research within the Lurie Center for Autism. As the principal investigator of the Bilbo Lab, Bilbo investigates how environmental challenges during the perinatal period impact the immune system and further influence brain development, cognition, and affective behaviors later in life..
Bilbo completed her undergraduate degree in psychology and biology at the University of Texas at Austin. [1] She received her Bachelor of Arts in 1998, graduating with high honors. [1] While Bilbo was at UT Austin, she conducted research on the role of the cholinergic system in learning in frogs. [2]
After her undergraduate degree, Bilbo joined the lab of Randy Nelson at Johns Hopkins University. [3] Bilbo completed her master's degree in 2000 and continued on to complete a PhD in Neuroendocrinology in Nelson's lab. [3]
Bilbo's graduate work was largely involving the importance of social and environmental factors in the regulation of sex specific and seasonal changes in immune response. [4] She published a paper how immune signalling influenced partner preferences in prairie voles in 1999, [5] and another on how sex hormones impact immune function in male and female Siberian Hamsters in 2001. [6] In 2002, Bilbo published a first author paper in the Proceedings of the Royal Society showing the effect of shortening photoperiods on the immune response of Siberian hamsters. [7] Following this finding, Bilbo explored how photoperiods predict environmental conditions and immune trafficking in anticipation of infection. [8] In 2002 Bilbo published a paper on the importance of melatonin in regulating immune response. [9] In 2003, Bilbo published a paper on the sex differences in immune responses to photoperiod modulation. [4]
After completing her graduate work, Bilbo pursued her postdoctoral work in neuroimmunology at the Center for Neuroscience at the University of Colorado in 2003. [3] Her research work here was concerned with the effects of neonatal bacterial infection on memory impairment in adult rats. [10] [11] [12] [13] In 2007, Bilbo was appointed to assistant professor of psychology and neuroscience at Duke University. [14] Bilbo remained on the faculty at Duke, leading the Developmental Neuroimmunology Lab until 2016. [15] During her time at Duke, Bilbo investigated neuroimmune interactions in brain development, [1] [16] and the effect of neonatal infection on glial cell biology and immune functions later in life. [17] [18]
In 2016, Bilbo joined the faculty at Harvard Medical School and became the Lurie Family Associate Professor of Pediatric and Neuroscience as well as the director of research for the Lurie Center for Autism at the Massachusetts General Hospital for Children. [15] During this time she did research on the effect of adolescent exposure to morphine on long-term microglial gene expression. [19] [20] She also studied the effect of environmental pollutant exposure during critical periods of prenatal development on metabolic, behavioral, and neuroinflammatory developments in adult offspring. [21] [22] In 2018, Bilbo and her lab studied the role of microglia in the regulation of social behavior in adolescent rats. [23] Following these findings, Bilbo wrote a review paper highlighting the understudied connections between the immune system, social behavior, and dopaminergic circuitry. [24]
Bilbo returned to Duke in July 2019 to hold the title of Haley Family Professor of Psychology and Neuroscience while still collaborating with the Lurie Center and other researchers in Boston. [10]
Bilbo remains active in the scientific community as an editorial board member for Brain, Behavior, and Immunity, an invited journal editor for Brain, Behavior, and Immunity, and as a previous guest editor for Hormones and Behavior. [25] Bilbo is also actively involved in outreach in the Duke community and recently gave a talk geared towards raising the visibility of female scientists and to encourage female participation in STEM. [26]
The Coolidge effect is a biological phenomenon seen in animals, whereby males exhibit renewed sexual interest whenever a new female is introduced, even after sex with prior but still available sexual partners. To a lesser extent, the effect is also seen among females with regard to their mates.
Glia, also called glial cells(gliocytes) or neuroglia, are non-neuronal cells in the central nervous system (brain and spinal cord) 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.
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.
HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. It is a syndrome of progressive deterioration of memory, cognition, behavior, and motor function in HIV-infected individuals during the late stages of the disease, when immunodeficiency is severe. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of HIV-associated dementia (HAD) are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss.
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.
A glial scar formation (gliosis) is a reactive cellular process involving astrogliosis that occurs after injury to the central nervous system. As with scarring in other organs and tissues, the glial scar is the body's mechanism to protect and begin the healing process in the nervous system.
Sickness behavior is a coordinated set of adaptive behavioral changes that develop in ill individuals during the course of an infection. They usually, but not always, accompany fever and aid survival. Such illness responses include lethargy, depression, anxiety, malaise, loss of appetite, sleepiness, hyperalgesia, reduction in grooming and failure to concentrate. Sickness behavior is a motivational state that reorganizes the organism's priorities to cope with infectious pathogens. It has been suggested as relevant to understanding depression, and some aspects of the suffering that occurs in cancer.
(+)-Naloxone (dextro-naloxone) is a drug which is the opposite enantiomer of the opioid antagonist drug (−)-naloxone. Unlike (-)-naloxone, (+)-naloxone has no significant affinity for opioid receptors, but instead has been discovered to act as a selective antagonist of Toll-like receptor 4. This receptor is involved in immune system responses, and activation of TLR4 induces glial activation and release of inflammatory mediators such as TNF-α and Interleukin-1.
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.
The development of an animal model of autism is one approach researchers use to study potential causes of autism. Given the complexity of autism and its etiology, researchers often focus only on single features of autism when using animal models.
Beth Stevens is an associate professor in the Department of Neurology at Harvard Medical School and the F. M. Kirby Neurobiology Center at Boston Children’s Hospital. She has helped to identify the role of microglia and complement proteins in the "pruning" or removal of synaptic cells during brain development, and has also determined that the impaired or abnormal microglial function could be responsible for diseases like autism, schizophrenia, and Alzheimer's.
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.
Anna V. Molofsky is an American psychiatrist and glial biologist. She is an associate professor in the department of psychiatry at UC San Francisco. Her lab currently studies the communication between astrocytes, microglia, and neurons to understand how these signals regulate synaptic development in health and disease.
Sabra Klein is an American microbiologist who is a Professor of Molecular Microbiology and Immunology at the Johns Hopkins Bloomberg School of Public Health. Her research considers how sex and gender impact the immune system. During the COVID-19 pandemic, Klein investigated why men and women have different COVID-19 outcomes.
Robyn S. Klein is an American neuroimmunologist as well as the Vice Provost and Associate Dean for Graduate Education at Washington University in St. Louis Missouri. Klein is also a professor in the Departments of Medicine, Anatomy & Neurobiology, and Pathology & Immunology. Her research explores the pathogenesis of neuroinflammation in the central nervous system by probing how immune signalling molecules regulate blood brain barrier permeability. Klein is also a fervent advocate for gender equity in STEM, publishing mechanisms to improve gender equity in speakers at conferences, participating nationally on gender equity discussion panels, and through service as the president of the Academic Women’s Network at the Washington University School of Medicine.
Erin M. Gibson is a glial and circadian biologist as well as an assistant professor in the Department of Psychiatry and Behavioral Sciences and the Stanford Center for Sleep Sciences and Medicine at Stanford University. Gibson investigates the role of glial cells in sculpting neural circuits and mechanistically probes how the circadian rhythm modulates glial biology.
Anne Schaefer is a neuroscientist, professor of Neuroscience, vice-chair of Neuroscience, and director of the Center for Glial Biology at the Icahn School of Medicine at Mount Sinai in New York City. Schaefer investigates the epigenetic mechanisms of cellular plasticity and their role in the regulation of microglia-neuron interactions. Her research is aimed at understanding the mechanisms underlying various neuropsychiatric disorders and finding novel ways to target the epigenome therapeutically.
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.
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.
Lindsay M. De Biase is an American neuroscientist and glial biologist as well as an assistant professor at the David Geffen School of Medicine at the University of California, Los Angeles. De Biase explores the diversity of microglia that exist within the basal ganglia circuitry to one day target regional or circuit-specific microglia in disease. De Biase's graduate work highlighted the existence and roles of neuron-OPC synapses in development and her postdoctoral work was critical in showing that microglia are not homogenous within the brain parenchyma.