INS NYC 2024 Program

Poster

Poster Session 04 Program Schedule

02/15/2024
12:00 pm - 01:15 pm
Room: Shubert Complex (Posters 1-60)

Poster Session 04: Neuroimaging | Neurostimulation/Neuromodulation | Teleneuropsychology/Technology


Final Abstract #59

Older APOE4 Carriers with Reduced Cerebrovascular Reactivity Exhibit High White Matter Hyperintensity Burden

Arunima Kapoor, University Of California, Irvine, IRVINE, United States
Shubir Dutt, University of Southern California, Los Angeles, United States
Belinda Yew, University of Southern California, Los Angeles, United States
Jung Jang, University Of California, Irvine, IRVINE, United States
John Paul Alitin, University Of California, Irvine, IRVINE, United States
Jean Ho, University Of California, Irvine, IRVINE, United States
Isabel Sible, University of Southern California, Los Angeles, United States
Anisa Marshall, University of Southern California, Los Angeles, United States
Fatemah Shenasa, University Of California, Irvine, IRVINE, United States
Allison Engstrom, University Of California, Irvine, IRVINE, United States
Aimee Gaubert, University Of California, Irvine, IRVINE, United States
Xingfeng Shao, University of Southern California, Los Angeles, United States
Danny Wang, University of Southern California, Los Angeles, United States
Kathleen Rodgers, University of Arizona, Tucson, United States
David Bradford, University of Arizona, Tucson, United States
Daniel Nation, University of Southern California, Los Angeles, United States

Category: Dementia (Alzheimer's Disease)

Keyword 1: vascular cognitive impairment
Keyword 2: apolipoprotein E
Keyword 3: cerebrovascular injury

Objective:

APOE4 carriers at genetic risk for Alzheimer’s disease exhibit cerebrovascular dysfunction relative to APOE3 homozygotes. Impaired cerebrovascular reactivity (CVR) may precipitate white matter damage in APOE4 carriers. No studies to date have examined the relationship between regional CVR and WMH burden in APOE4 carriers.  We hypothesized that older APOE4 carriers with diminished CVR would exhibit higher WMH burden.

Participants and Methods:

Seventy-eight independently living older adults (mean age = 69.2 years; SD = 8.2; age range 55-89 years; 37.2% male) free of dementia or clinical stroke were recruited from the community and underwent brain MRI. Pseudo-continuous arterial spin labeling MRI quantified whole brain and region-of-interest (ROI) cerebral perfusion during CVR to hypercapnia and hypocapnia. WMH volume was determined using the lesion growth algorithm implemented in the LST toolbox. APOE genotyping was conducted on blood samples.

Results:

Hierarchical regression analysis revealed a significant association between whole brain CVR to hypercapnia and WMH [B = -.02, 95% CI (-.04, -.002), p = .028], adjusting for age, sex and intracranial volume. Analyses stratified by APOE4 status revealed a significant association between whole brain CVR to hypercapnia and WMH burden in the APOE4 carriers (B = -.04, 95% CI (-.07, -.01), p = .008), but not non-carriers. ROI analysis indicated CVR in temporal and parietal regions correlated with WMH burden in APOE4 carriers, but not non-carriers. CVR to hypocapnia was not associated with WMH burden.  

Conclusions:

Findings suggest deficits in cerebral vasodilatory capacity are associated with WMH burden, specifically in temporal and parietal regions in APOE4 carriers. Cerebral vasoconstrictive response to hypocapnia is not associated with WMH burden. Further longitudinal studies are warranted to examine cerebrovascular deficits contributing to WMH burden in APOE4 carriers.