Michael Chumley
Professor Texas Christian University
- Fort Worth TX
Research focus has been on the role of inflammation in neurodegenerative diseases.
Media
Social
Biography
Michael has a rich history in mentoring graduate and undergraduate students. These students learn a number of molecular and cellular techniques such as numerous types of immunoassays, gene expression studies, histology and microscopy, and cell culture work. Students also may be involved with animal husbandry and behavioral and cognitive testing.
Areas of Expertise
Accomplishments
Wassenich Award for Mentoring in the TCU Community
2014
John V. Roach Honors College Professor of the Year
2013
Education
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
Affiliations
- Psychoneuroimmunology Research Society
- American Association for the Advancement of Science
- Society for Neuroscience
Media Appearances
The Neurobiology of Aging
TCU Magazine online
2015-09-23
Three professors in TCU’s College of Science and Engineering are using the tools of their respective academic disciplines to research the disease. Associate professor of biology Michael Chumley, assistant professor of chemistry Kayla Green and associate professor of psychology Gary Boehm formed the Neurobiology of Aging Collaborative to study the amyloid beta proteins associated with Alzheimer’s disease. They are researching how the proteins form and impair cognition as well as how that formation process might be interrupted.
Faculty Q & A: Michael Chumley
TCU Magazine online
2015-03-20
At the 142nd Convocation in September, the associate professor of biology received the Wassenich Award for Mentoring in the TCU community.
Event Appearances
Panelist
(2022) Society for Neuroscience San Diego, CA
Attendee
(2019) Society for Neuroscience Chicago, IL
Attendee
(2018) Society for Neuroscience San Diego, CA
Speaker
(2018) Keystone Symposium Keystone, CO
Attendee
(2017) Keystone Symposium Keystone, CO
Panelist
(2017) Psychoneuroimmunology Research Society Galveston, TX
Research Grants
Building better antioxidants: virtual screening, synthesis, and characterization of multifunctional small molecules combining Nrf2 pathway activation and direct antioxidant activity,
National Institutes of Health
2022
Targeting oxidative stress in neurodegeneration using pyridol-derived small molecules,
National Institutes of Health
2018
Articles
A Synthetic Formula Amino Acid Diet Leads to Microbiome Dysbiosis, Reduced Colon Length, Inflammation, and Altered Locomotor Activity in C57BL/6J Mice
Microorganisms2023
The effects of synthetic, free-amino acid diets, similar to those prescribed as supplements for (phenylketonuria) PKU patients, on gut microbiota and overall health are not well understood. n the current, multidisciplinary study, we examined the effects of a synthetically-derived, low-fiber, amino acid diet on behavior, cognition, gut microbiome composition, and inflammatory markers.
Chronic sleep restriction increases soluble hippocampal Aβ-42 and impairs cognitive performance
Physiology & Behavior2020
Currently, over 44 million people worldwide suffer from Alzheimer's disease (AD). A common feature of AD is disrupted sleep. Sleep is essential for many psychological and physiological functions, though 35.3% of adults report getting less than 7 hours per night. The present research examined whether chronic sleep restriction would elevate hippocampal amyloid-beta1–42 expression or alter cognitive ability in adult C57BL/6 mice.
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.
