Michael Chumley 
Associate Professor | Texas Christian University
Fort Worth, TX, UNITED STATES
Research focus has been on the role of inflammation in neurodegenerative diseases.
Biography
Since arriving at TCU in 2008, my research focus has been on the role of inflammation in neurodegenerative diseases. I approach this research using a background in Exercise Physiology (M.S. 1994) and Immunology (Ph.D. 2000), and several years of post-doctoral research in developmental neurobiology. In conjunction with Dr. Gary Boehm of the Department of Psychology, we have formed the Neurobiology of Aging Collaborative, to investigate numerous age-related stressors and their affect on the nervous system.
Areas of Expertise (5)
Neurodegenerative Diseases
Developmental Neurobiology
Exercise Physiology
Immunology
Psychology
Education (3)
University of Colorado, Health Sciences Center: Ph.D., Immunology 2000
University of Wyoming: M.S., Exercise Physiology 1994
University of Wyoming: B.S., Education 1987
Links (3)
Research Grants (3)
Pyridol derived small molecules targeting oxidative stress,
National Institutes of Health R15 $376,045
2015
Assessing the in vivo effects of pyridol derived small molecules
Alzheimer’s Association New Research Grant $997,924
2015
Pyridol derived small molecules targeting oxidative stress in neurodegeneration
National Institutes of Health R15 $390,161
2014
Articles (5)
Prolonged isolation stress accelerates the onset of Alzheimer’s disease-related pathology in 5xFAD mice despite running wheels and environmental enrichment
Behavioural Brain Research2019 Research has demonstrated that stress can exacerbate AD pathology in transgenic mouse models of AD. The purpose of the present studies was to extend this work by determining whether a social stressor, isolation stress, would increase the number of Aβ plaques in 5xFAD + transgenic mice in comparison to group-housed controls, and accelerate the onset of cognitive deficits in contextual fear-conditioning.
Intraventricular murine Aβ infusion elicits hippocampal inflammation and disrupts the consolidation, but not retrieval, of conditioned fear in C57BL6/J mice
Behavioural Brain Research2019 Although one of the defining characteristics of Alzheimer’s disease is the presence of amyloid-beta (Aβ) plaques, the early accumulation of soluble Aβ oligomers (AβOs) may disrupt synaptic function and trigger cognitive impairments long before the appearance of plaques.
The α5-GABAAR inverse agonist MRK-016 upregulates hippocampal BDNF expression and prevents cognitive deficits in LPS-treated mice, despite elevations in hippocampal Aβ
Behavioural Brain Research2018 Alzheimer’s disease is marked by the presence of amyloid-beta (Aβ) plaques, elevated central cytokine levels, dysregulation of BDNF-related gene expression, and cognitive decline. Previously, our laboratory has demonstrated that repeated administration of peripheral LPS is sufficient to significantly increase the presence of central Aβ in the hippocampus, and that this upregulation corresponds with deficits in learning and memory.
Effects of social isolation on LPS-induced hippocampal amyloid-beta expression and cognitive dysfunction in C57BL6/J mice
Brain Behavior and Immunity2017 The connection between inflammation and various disease states is strongly affirmed in the existing literature, along with the connection between stress and immune function. Of particular interest is the connection between psychological stress and Alzheimer’s disease (AD), as clinical data have shown that stress is a risk factor for dementia-related dysfunction.
Prior exposure to repeated peripheral LPS injections prevents further accumulation of hippocampal beta-amyloid
Brain, Behavior, and Immunity2017 Alzheimer’s disease (AD) is characterized by the accumulation of beta-amyloid plaques and neurofibrillary tangles. Our laboratory has previously demonstrated that repeated bouts of LPS-induced inflammation increase beta-amyloid within the hippocampus of non-transgenic mice.
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