Abstract
Biomarkers have the potential to aid in the study of Alzheimer’s disease (AD); unfortunately, AD biomarker values often have a high degree of overlap between healthy and AD individuals. This study investigates the potential utility of a series of novel AD biomarkers, the sixty second 129Xe retention time, and the xenon washout parameter, based on the washout of hyperpolarized 129Xe from the brain of AD participants following inhalation. The xenon washout parameter is influenced by cerebral perfusion, T1 relaxation of xenon, and the xenon partition coefficient, all factors influenced by AD. Participants with AD (n = 4) and healthy volunteers (n = 4) were imaged using hyperpolarized 129Xe magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) to determine the amount of retained xenon in the brain. At 60 s after the breath hold, AD patients retained significantly higher amounts of 129Xe compared to healthy controls. Data was fit to a pharmacokinetic model and the xenon washout parameter was extracted. Xenon washout in white and grey matter occurs at a slower rate in Alzheimer’s participants (129Xe half-life time of 42 s and 43 s, respectively) relative to controls (20 s and 16 s, respectively). Following larger scale clinical trials for validation, the xenon washout parameter has the potential to become a useful biomarker for the support of AD diagnosis.
Highlights
Alzheimer’s disease (AD) is an age-related neurodegenerative disorder that compromises the memory and executive function of affected individuals [1]
We demonstrate the preliminary results of two potential biomarkers of AD based on the washout of HP 129 Xe from the brain of AD participants, which was detected using 129 Xe magnetic resonance spectroscopy (MRS)
This research study was approved by the research ethics boards (REB) of Lakehead University (LU) and the Thunder Bay Regional Health Sciences Centre (TBRHSC) (Reference number RP-307)
Summary
Alzheimer’s disease (AD) is an age-related neurodegenerative disorder that compromises the memory and executive function of affected individuals [1]. While the amyloid cascade hypothesis and its variants [7,19,20,21]. Remain the favored AD hypothesis, the exact cause of AD remains contentious [22,23,24,25]. Cerebro-vascular factors have been demonstrated to both influence and to be influenced by AD pathology [26,27,28]. These vascular effects include an increased risk of stroke in AD patients [29]. A history of strokes excludes a diagnosis of AD in favor of vascular dementia [30]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
