Courses: Abnormal (Psyc 306), Health (Psyc 360), Intro (Psyc 107), Grad Health (Psyc 630)
E-mail: M-Meagher@tamu.edu
Research Interests:
Current Research:
My research focuses on the role of stress and emotion in health, with an emphasis on pain and immune-related diseases. My pain research program uses both animal and human models to examine how stress and emotion alter pain reactivity and perception, as well as the neural substrates of affective pain modulation. We use a range of laboratory pain procedures, psychophysical testing procedures, and emotion induction procedures to study how emotion alters pain processing in humans. Our most recent research investigates the impact of written emotional disclosure of traumatic life events on laboratory pain. Animal models are also used to examine the neural systems that underlie affective pain modulation and the emotional component of pain. My psychoneuroimmunology research program examines how psychosocial stressors alter immune processes and vulnerability to an animal model of multiple sclerosis, Theiler's murine encephalomyelitis virus infection. An integrative approach is employed to study the interaction between behavioral, endocrine, and immune systems. Animal models of social and restraint stress are used to investigate the effects of neuroendocrine responses on cytokine and chemokine expression and illness behaviors during Theiler's virus infection. Another novel aspect of my research program is that it examines the effects of early maternal deprivation on vulnerability to infection later in life. The long-term goal of this project is to elucidate the mechanisms by which early life stress alters susceptibility to later infectious, inflammatory, and autoimmune diseases. Understanding these mechanisms could lead to interventions that prevent or reverse the deleterious effects of early life stress on disease predisposition.
Finally, I am collaborating on a project that investigates the effects of age-related changes in basal forebrain cholinergic neurons and associated changes in memory. Basal forebrain damage has been linked to clinical symptoms of Alzheimer's disease in humans. The goal of this project is to identify the cellular and molecular mechanisms responsible for age-related changes in cellular and memorial function. The elucidation of these mechanisms may lead to the development of pharmacological interventions that prevent or alleviate age-related pathologies.