BIOMARKERS - Poster Presentation - The Influence of Vascular Function on Biomarkers for Alzheimer’s Disease in Adults with Chronic Cerebral Hypoperfusion

Sep 30, 2026

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Background: Cerebral hypoperfusion contributes to cognitive decline and increases Alzheimer’s disease (AD) risk, with vertebral artery hypoplasia (VAH) linked to reduced cerebral blood flow and higher cerebral pulsatility. Higher blood pressure and arterial stiffness may further elevate pulsatility and influence neurodegeneration. Objective: evaluate how BP and arterial stiffness affect pulsatility and neurodegeneration biomarkers in adults with and without VAH. Methods used 4D flow MRI, arterial stiffness testing, and serum biomarker assays.

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Abstract

Background

Methods

Results

Conclusions

DOI: 10. 1002/alz70856_106791 BIOMARKERS POSTER PRESENTATION BIOMARKERS (NON-NEUROIMAGING) The Influence of Vascular Function on Biomarkers for Alzheimer’s Disease in Adults with Chronic Cerebral Hypoperfusion Brandon G. Fico1, 2 Nicole A. Loggie 1 M. Erin Moir 1 Sarean HarmoniA. Gaynor-Metzinger 1 Alexander M. Norby 1 Anna J. Howery 1 Alexandre Hamaide2 Leonardo A. Rivera-Rivera3 Oliver Wieben 1 Kevin M. Johnson3 Sterling C Johnson3 Jill N. Barnes 1 1 University of Wisconsin-Madison, Madison, WI, USA 2 Florida Atlantic University, Boca Raton, FL, USA 3Wisconsin Alzheimer’s Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA Correspondence Brandon G. Fico, University of Wisconsin-Madison, Madison, WI, USA. [Email:](Email: bfico@fau.edu)[ bfico@fau.edu](Email: bfico@fau.edu) Abstract Background: Cerebral hypoperfusion can result in cognitive decline and is a risk factor forAlzheimer’s disease(AD). A common cerebral anatomical variation(vertebral artery hypoplasia [VAH]) has been linked to reduced cerebral blood flow and elevated cerebral pulsatility. Additionally, increased blood pressure (BP) and arterial stiffness are associated with elevated cerebral pulsatility and may increase risk for neurodegeneration and AD in those with VAH. Therefore, the purpose of this study was to determine the influence of BP and arterial stiffness on cerebral pulsatility and biomarkers for neurodegeneration andAD in adults with and without VAH. Methods: Sixty-five cognitively unimpaired healthy older adults (64±4 years; 52 females) with VAH (n = 17) and without VAH (noVAH; n = 48) were included in the study. Brachial BP, arterial stiffness (carotid-femoral pulse wave velocity), serum blood samples, and 3T magnetic resonance imaging (MRI) were assessed. Serum samples were analyzed for neurofilament light chain (NfL) and phospho-tau 217 (pTau 217). Intracranial pulsatility index (PI) was quantified using 4D flow MRI in the internal carotid arteries (ICAs), anterior cerebral arteries (ACAs), middle cerebral arteries (MCAs), vertebral arteries (VAs), and basilar artery (BA). Results: There were no group differences in BP, arterial stiffness, or cerebral PI (in the ICAs, MCAs, VAs, and BA) between VAH and noVAH (p >0.05 for all). However, the VAH group had greaterACAsPI(p <0.01)compared with the noVAH group. Systolic BP was positively associated with cerebral PI in the MCAs in theVAH group only (r=0. 63, p <0.01), as there was no association in the noVAH group(r=0.08, p = 0. 60). There were no differences in serum NfL or pTau 217 biomarkers between VAH and noVAH groups This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2025 The Alzheimer’s Association. Alzheimer’s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer’s Association. Alzheimer’s Dement. 2025;21(Suppl. 2):e106791. [https://doi.org/10.1002/alz70856_106791](https://doi.org/10.1002/alz70856_106791) wi[leyonlinelibrary.com/journal/alz](leyonlinelibrary.com/journal/alz) 1of2 BIOMARKERS (p >0.05 for both). In addition, systolic BP was inversely associated with pTau 217 (r= - 0.80, p <0.01) in the VAH group only, as there was no association in the noVAH group (r=-0.04, p >0.83). Conclusions: Adults with VAH had greater cerebral pulsatility in the anterior circulation compared with adults without VAH. In adults with VAH, increased systolic BP resulted in elevated cerebral pulsatility and potentially acting as a compensatory mechanism for decreased perfusion pressure, the increased systolic BP resulted in a reduction in pTau 217 levels.

FAQs

What is the study’s main purpose?

To determine how blood pressure and arterial stiffness influence cerebral pulsatility and neurodegeneration biomarkers in adults with and without vertebral artery hypoplasia (VAH).

How were cerebral pulsatility and biomarkers measured?

Cerebral pulsatility index was quantified with 4D flow MRI in multiple arteries, while serum samples were analyzed for neurofilament light chain (NfL) and phospho-tau 217 (pTau 217).

What were the key results comparing VAH and noVAH groups?

No group differences were found in BP, arterial stiffness, or cerebral pulsatility overall, but the VAH group showed greater ACAs pulsatility. Serum NfL and pTau 217 did not differ between groups.

What do the conclusions suggest about systolic blood pressure and AD-related biomarkers in VAH?

In the VAH group, increased systolic BP was associated with higher cerebral pulsatility and was also linked to lower pTau 217 levels, suggesting possible compensatory mechanisms.

Sep 30, 2026

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