Abstract Details

Title Circulating Inflammatory Biomarkers and Enlarged Perivascular Spaces: the Framingham Heart Study

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P1 - Poster Session 1 (9:00 AM-5:00 PM)

Poster/Presentation
Number 128

Objective To determine the association between circulating biomarkers of inflammation and enlarged perivascular spaces (EPVS).

Background Elevated levels of systemic inflammatory markers are associated with stroke and dementia. The pathogenesis of these associations may involve cerebral small vessel disease (CSVD) and glymphatic dysfunction, both of which are represented in measurements of EPVS.

Design/Methods

Framingham Offspring Cohort participants with available biomarkers and brain MRI were included. EPVS were rated using validated methods, and characterized in the basal ganglia (BG), centrum semiovale (CSO), and with a mixed score reflecting high burden in both regions. We used multivariable ordinal logistic regression analyses to relate 15 biomarkers representing systemic inflammation, vascular inflammation, and oxidative stress to EPVS burden. The primary model was adjusted for age, sex and time interval from biomarker ascertainment to MRI. Additional models were also adjusted for vascular risk factors.

Results We included 1035 participants with 1533 MRI (mean age 65 ± 9 years, 47% men). High circulating levels of several biomarkers were related to high burden of EPVS: interleukin-6 (odds ratio [OR] 1.14, 95% confidence interval [CI] 1.03-1.26), P selectin (OR 1.26, 95%CI 1.17-1.42), Osteoprotegerin (OR 1.21, 95% CI 1.07-1.37) and intercellular adhesion molecule 1 (OR 1.20, 95%CI 1.08-1.33) with for BG region; P-selectin (OR1.13, 95% CI 1.02-1.27) in the CSO region; and Osteoprotegerin with mixed location EPVS after adjustment for vascular risk factors (OR 1.17, 95% CI 1.01-1.35).

Conclusions Our study suggests that inflammation may be play a role in the pathogenesis of CSVD and glymphatic dysfunction represented by ePVS. Future studies will clarify the potential role of ePVS as mediators in the pathway from inflammation to adverse cognitive outcomes and stroke.

Authors/Disclosures
Oluchi S. Ekenze PRESENTER	Ms. Ekenze has nothing to disclose.
	No disclosure on file
	No disclosure on file
	No disclosure on file
	No disclosure on file
Charles S. DeCarli, MD, FAAN (UC Davis Health - Dept of NeurologyAlzheimer's Disease Research Center)	Dr. DeCarli has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Novo Nordisk. The institution of Dr. DeCarli has received research support from NIH.
Sudha Seshadri, MD, FAAN (Glenn Biggs Institute for Alzheimer'S and Neurodegenerative Diseases)	Dr. Seshadri has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Eisai. Dr. Seshadri has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Biogen. The institution of Dr. Seshadri has received research support from NIH. The institution of Dr. Seshadri has received research support from Alzheimer Association.
Jose R. Romero, MD (Boston University School of Medicine - Boston Medical Center)	The institution of Dr. Romero has received research support from NIH/NIA.

��ɫ��

��ɫ��