Determination of Acrolein-Associated T1 and T2 Relaxation Times and Noninvasive Detection Using Nuclear Magnetic Resonance and Magnetic Resonance Spectroscopy
- Authors: Vike N.1, Tang J.2, Talavage T.2,3, Shi R.1,2, Rispoli J.2,3,4
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Affiliations:
- Department of Basic Medical Sciences, Purdue University
- Weldon School of Biomedical Engineering, Purdue University
- School of Electrical and Computer Engineering, Purdue University
- Center for Cancer Research, Purdue University
- Issue: Vol 50, No 11 (2019)
- Pages: 1291-1303
- Section: Original Paper
- URL: https://journals.rcsi.science/0937-9347/article/view/248686
- DOI: https://doi.org/10.1007/s00723-019-01148-2
- ID: 248686
Cite item
Abstract
An estimated 3.3 million people are living with a traumatic brain injury (TBI)-associated morbidity. Currently, only invasive and sacrificial methods exist to study neurochemical alterations following TBI. Nuclear magnetic resonance methods—magnetic resonance imaging (MRI) and spectroscopy (MRS)—are powerful tools which may be used noninvasively to diagnose a range of medical issues. These methods can be utilized to explore brain functionality, connectivity, and biochemistry. Unfortunately, many of the commonly studied brain metabolites (e.g., N-acetyl-aspartate, choline, creatine) remain relatively stable following mild to moderate TBI and may not be suitable for longitudinal assessment of injury severity and location. Therefore, a critical need exists to investigate alternative biomarkers of TBI, such as acrolein. Acrolein is a byproduct of lipid peroxidation and accumulates following damage to neuronal tissue. Acrolein has been shown to increase in post-mortem rat brain tissue following TBI. However, no methods exist to noninvasively quantify acrolein in vivo. Currently, we have characterized the T1 and T2 of acrolein via nuclear magnetic resonance saturation recovery and Carr–Purcell–Meiboom–Gill experiments, accordingly, to maximize the signal-to-noise ratio of acrolein obtained with MRS. In addition, we have quantified acrolein in water and whole-brain phantom using PRESS MRS and standard post-processing methods. With this potential novel biomarker for assessing TBI, we can investigate methods for predicting acute and chronic neurological dysfunction in humans and animal models. By quantifying and localizing acrolein with MRS, and investigating neurological outcomes associated with in vivo measures, patient-specific interventions could be developed to decrease TBI-associated morbidity and improve quality of life.
About the authors
Nicole Vike
Department of Basic Medical Sciences, Purdue University
Email: jrispoli@purdue.edu
United States, West Lafayette, IN, 47907
Jonathan Tang
Weldon School of Biomedical Engineering, Purdue University
Email: jrispoli@purdue.edu
United States, West Lafayette, IN, 47907
Thomas Talavage
Weldon School of Biomedical Engineering, Purdue University; School of Electrical and Computer Engineering, Purdue University
Email: jrispoli@purdue.edu
United States, West Lafayette, IN, 47907; West Lafayette, IN, 47907
Riyi Shi
Department of Basic Medical Sciences, Purdue University; Weldon School of Biomedical Engineering, Purdue University
Author for correspondence.
Email: riyi@purdue.edu
United States, West Lafayette, IN, 47907; West Lafayette, IN, 47907
Joseph Rispoli
Weldon School of Biomedical Engineering, Purdue University; School of Electrical and Computer Engineering, Purdue University; Center for Cancer Research, Purdue University
Author for correspondence.
Email: jrispoli@purdue.edu
ORCID iD: 0000-0003-4514-3390
United States, West Lafayette, IN, 47907; West Lafayette, IN, 47907; West Lafayette, IN, 47907