Differentiating Small Vessel Disease (SVD) from Neurodegenerative Dementia (Alzheimer’s Disease) using Arterial Spin Labeling MRI - a Feasibility Study
Lindsay Wanner1, Jason Badelita1, Lucy Conser1, Irene George1, Bryant Hartman1, Harrison Kline1, Davis Melin1, Pranav Pradhan1, Charles Joseph1
1Liberty University College of Osteopathic Medicine
Objective:

Develop a 3D Arterial Spin Labeling (ASL) MRI biomarker detection technique to potentially distinguish SVD from neurodegenerative dementia before significant disease progression.

Background:

SVD and neurodegenerative dementia are clinically indistinguishable and difficult to differentiate with conventional MRI. Both exhibit decline of capillary integrity and cognition, resulting from blood-brain-barrier (BBB) breakdown and subsequent leak. However, the consequence of BBB leak may be mechanistically divergent. SVD causes major changes in the perfusion paradigm, potentially resulting in reduced arterial mean transit time (aMTT) and capillary mean transit time (cMTT). Neurodegenerative dementia exhibits normal aMTT but prolonged cMTT. We hypothesize a shared underlying pathophysiology on a shared disease spectrum. 

Design/Methods:

Twenty-one subjects with no dementia (n=7), Alzheimer’s (n=7) or Vascular Dementia (n=7), and Montreal Cognitive Assessment scores between 10 and 17 were recruited. Subjects underwent a 3T Skyra magnet MRI scan using 3D ASL sequencing. Average signal intensities were recorded in 6 brain regions: homologous bitemporal, biparietal, and bi-frontal regions. Early and late phases of perfusion were graphed to compare time to max arterial peak perfusion, amplitude between groups, and linear clearance rate of the late phase of perfusion.

Results:
 Average arterial perfusion signal strength at 800, 1000, 1200, 1400, and 1600 ms post arterial spin labeling in each region between all groups showed no significant difference. Late phase perfusion (2800-4000ms) in both dementia groups showed highly significant differences (p≤0.04) from controls in all affected areas except the right parietal lobe. There are no regions where perfusion between dementia groups differed significantly. 
Conclusions:

This technique is unable to differentiate arterial phase perfusion changes in either affected group from normal controls or each other. This may be related to either limitations in technique or absence in arteriolar pathology. The latter possibility suggests that both entities share the same inciting initial BBB pathology. 

10.1212/WNL.0000000000208940
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