A pilot cohort study of blood brain barrier permeability in Alzheimer’s disease using dynamic contrast enhanced magnetic resonance imaging
Abstract
Blood–brain barrier (BBB) dysfunction is implicated as a key link between neuroinflammation and neurodegeneration in Alzheimer’s disease (AD). Peripheral inflammation may exacerbate cognitive decline by promoting BBB breakdown and impairing clearance of amyloid and tau, yet in vivo evidence for this hypothesis remains limited. We conducted a pilot cohort study to assess the feasibility of utilising dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) to quantify BBB permeability in AD, and to explore associations with cognitive decline, peripheral inflammation, and neurodegeneration. Fourteen participants with clinically diagnosed AD and 16 matched controls underwent baseline clinical, blood, urine, and DCE-MRI assessments. Thirteen AD participants were clinically reassessed after 12 months. BBB permeability was quantified using Patlak modelling in whole brain, grey and white matter, and selected regions of interest. Serum cytokines, phosphorylated tau-181 (pTau-181), neurofilament light (NfL), and urinary neopterin were analysed. BBB permeability did not differ significantly between AD and controls across global or regional measures at baseline. However, higher baseline permeability in the left entorhinal cortex was significantly associated with greater cognitive decline over 12 months. AD participants exhibited elevated serum interferon-γ relative to controls, and higher baseline interleukin-6 was associated with faster cognitive decline. This pilot study supports feasibility of regional DCE-MRI measurement in people with AD. Larger biomarker-confirmed cohorts are warranted to evaluate prognostic utility and to clarify the interaction between peripheral inflammation, BBB dysfunction and clinical progression in AD.
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BibTeX
@article{mccausland2026pilot,
title = {{A pilot cohort study of blood brain barrier permeability in Alzheimer’s disease using dynamic contrast enhanced magnetic resonance imaging}},
author = {Beth Mary Stevens McCausland and Aravinthan Varatharaj and Nathan Thomas Matthew Huneke and Steevo Abraham and Rana Abadalkareem and Bartholomew Thomas and Claire Louise Gee and Amy Patricia Kunicki and Angela Darekar and Jessica L. Teeling and Henrik Zetterberg and Ian Galea and Jay Amin},
journal = {Scientific Reports},
year = {2026},
month = oct,
doi = {10.1038/s41598-026-71888-2},
url = {https://www.nature.com/articles/s41598-026-71888-2},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - A pilot cohort study of blood brain barrier permeability in Alzheimer’s disease using dynamic contrast enhanced magnetic resonance imaging
AU - Beth Mary Stevens McCausland
AU - Aravinthan Varatharaj
AU - Nathan Thomas Matthew Huneke
AU - Steevo Abraham
AU - Rana Abadalkareem
AU - Bartholomew Thomas
AU - Claire Louise Gee
AU - Amy Patricia Kunicki
AU - Angela Darekar
AU - Jessica L. Teeling
AU - Henrik Zetterberg
AU - Ian Galea
AU - Jay Amin
PY - 2026
DA - 2026/10/26
JO - Scientific Reports
DO - 10.1038/s41598-026-71888-2
UR - https://www.nature.com/articles/s41598-026-71888-2
AB - Blood–brain barrier (BBB) dysfunction is implicated as a key link between neuroinflammation and neurodegeneration in Alzheimer’s disease (AD). Peripheral inflammation may exacerbate cognitive decline by promoting BBB breakdown and impairing clearance of amyloid and tau, yet in vivo evidence for this hypothesis remains limited. We conducted a pilot cohort study to assess the feasibility of utilising dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) to quantify BBB permeability in AD, and to explore associations with cognitive decline, peripheral inflammation, and neurodegeneration. Fourteen participants with clinically diagnosed AD and 16 matched controls underwent baseline clinical, blood, urine, and DCE-MRI assessments. Thirteen AD participants were clinically reassessed after 12 months. BBB permeability was quantified using Patlak modelling in whole brain, grey and white matter, and selected regions of interest. Serum cytokines, phosphorylated tau-181 (pTau-181), neurofilament light (NfL), and urinary neopterin were analysed. BBB permeability did not differ significantly between AD and controls across global or regional measures at baseline. However, higher baseline permeability in the left entorhinal cortex was significantly associated with greater cognitive decline over 12 months. AD participants exhibited elevated serum interferon-γ relative to controls, and higher baseline interleukin-6 was associated with faster cognitive decline. This pilot study supports feasibility of regional DCE-MRI measurement in people with AD. Larger biomarker-confirmed cohorts are warranted to evaluate prognostic utility and to clarify the interaction between peripheral inflammation, BBB dysfunction and clinical progression in AD.
SN - 2045-2322
ER -