Author(s): Timothy Kochany
Mentor(s): Jane Flinn, Psychology
AbstractTraumatic brain injuries (TBIs) are a major health concern, with there being over 200,000 TBI related hospitalizations in 2020. Repetitive mild TBIs (rmTBIs) lead to cumulative effects, worsening damage. Previous research demonstrated that young blood plasma transfusions may reverse factors of neurodegeneration in older populations, those with Alzheimer’s Disease, and those with TBIs.
Glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are proteins that act as biochemical markers that can be detected in blood to observe astrocyte activation and axonal integrity. Previous studies have shown that TBIs can induce neuronal death and contribute to neurodegenerative disease.
GFAP is a protein expressed by astrocytes that is involved in the injury repair of brain tissue. Overexpression of GFAP has been shown to correlate with lesion volume and TBI severity, as well as astrogliosis in releasing inflammatory mediators, such as cytokines and reactive oxygen species (ROS). This is part of the process of secondary injury during rmTBI. Neuroinflammation is a factor that contributes to neurodegeneration. This is pertinent because GFAP has been known to reflect glial responses to neuroinflammation.
Similarly, NfL is a protein found in the axon of neurons and is released into the plasma when injury or neurodegeneration is present. NfL is involved with structural support and aids in the conduction speed of action potentials. In previous studies, elevated levels of GFAP and NfL have been shown to signal the progression of neurodegeneration.
Audio TranscriptGlial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are proteins that act as biochemical markers that can be detected in blood to observe astrocyte activation and axonal integrity. Previous studies have shown that TBIs can induce neuronal death and contribute to neurodegenerative disease.
GFAP is a protein expressed by astrocytes that is involved in the injury repair of brain tissue. Overexpression of GFAP has been shown to correlate with lesion volume and TBI severity, as well as astrogliosis in releasing inflammatory mediators, such as cytokines and reactive oxygen species (ROS). This is part of the process of secondary injury during rmTBI. Neuroinflammation is a factor that contributes to neurodegeneration. This is pertinent because GFAP has been known to reflect glial responses to neuroinflammation.
Similarly, NfL is a protein found in the axon of neurons and is released into the plasma when injury or neurodegeneration is present. NfL is involved with structural support and aids in the conduction speed of action potentials. In previous studies, elevated levels of GFAP and NfL have been shown to signal the progression of neurodegeneration.
Hi everyone. My name is Tim Kochany. I’m a third-year neuroscience student at George Mason University and my project is The Effects of Young Blood Plasma on Neurofilament Light Chain and Glial Fibrillary Acidic Protein following Traumatic Brain Injury Administration in Wild-type mice. In the year 2020 alone, there have been reported over 200,000 hospitalizations related to traumatic brain injuries. This is a major world health concern because traumatic brain injuries have been known to lead to neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, as well as cognitive decline. Previous research has demonstrated that plasma from young mice injected into older mice has seemed to rescue deficits induced by traumatic brain injuries. My research focuses on two proteins that are involved in this process: Glial Fibrillary Acidic Protein, or GFAP, and Neurofilament Light Chain, or NfL. Glial Fibrillary Acidic Protein is a protein that is expressed by astrocytes and is involved in the injury repair process of the brain. Similarly, Neurofilament Light Chain is a protein found in axons, which is a part of the neuron that helps propagate the signal from one neuron to the next, and overexpression of this protein has been shown to signal the progression of neurodegeneration. Repetitive mild traumatic brain injuries lead to cumulative effects, worsening brain damage. Prior to the current study, plasma injections and saline injections have been administered and the mice have been euthanized and plasma samples have been collected. There are four groups of mice: TBI plasma, TBI saline, sham plasma, and sham saline. Sham is if no TBI has been administered. For the procedure, I am going to be looking at and I’m going to be using Enzyme-linked Immunosorbent Assay or ELISA to detect protein quantities in the plasma from these mice. For this process, antibodies for the specific protein are going to bind to that protein and then we are going to detect protein concentrations by shining a specific wavelength of light through the sample. My hypothesis is that traumatic brain injuries will increase levels of both GFAP and NfL, with the groups receiving plasma injections slightly lowering these concentrations. This research has significant implications for the study of neurodegeneration and public health relating to traumatic brain injury treatment. Unfortunately, no results are available at this time, as I’ve had errors with our ELISA microplate reader malfunctioning to collect data. However, data will be available at the OSCAR poster celebration on May 6. If you would like to see a full list of my works cited, you can scan this QR code here.
One reply on “The Effects of Young Blood Plasma on NfL and GFAP following Traumatic Brain Injury Administration in Wild-type Mice”
Cool topic. We need to understand so much more about the brain.