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Adverse Vascular Risk Relates to Cerebrospinal Fluid Biomarker Evidence of Axonal Injury in the Presence of Alzheimer's Disease Pathology

Journal article
Authors K. E. Osborn
J. M. Alverio
L. Dumitrescu
K. R. Pechman
K. A. Gifford
T. J. Hohman
Kaj Blennow
Henrik Zetterberg
A. L. Jefferson
Published in Journal of Alzheimers Disease
Volume 71
Issue 1
Pages 281-290
ISSN 1387-2877
Publication year 2019
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 281-290
Language en
Links dx.doi.org/10.3233/jad-190077
Keywords Alzheimer's disease, cerebrovascular, neurodegeneration, neurofilament light, vascular risk, white-matter lesions, silent brain infarcts, cognitive decline, a-beta, interstitial fluid, cigarette-smoking, older-adults, neurofilament, dementia, disorders, Neurosciences & Neurology
Subject categories Neurosciences

Abstract

Background: Vascular risk factors promote cerebral small vessel disease and neuropathological changes, particularly in white matter where large-caliber axons are located. How Alzheimer's disease pathology influences the brain's vulnerability in this regard is not well understood. Objective: Systemic vascular risk was assessed in relation to cerebrospinal fluid concentrations of neurofilament light, a biomarker of large-caliber axonal injury, evaluating for interactions by clinical and protein markers of Alzheimer's disease. Methods: Among Alzheimer's Disease Neuroimaging Initiative participants with normal cognition (n = 117), mild cognitive impairment (n = 190), and Alzheimer's disease (n = 95), linear regression related vascular risk (as measured by the modified Framingham Stroke Risk Profile) to neurofilament light, adjusting for age, sex, education, and cognitive diagnosis. Interactions were assessed by cognitive diagnosis, and by cerebrospinal fluid markers of A beta(42), hyperphosphorylated tau, and total tau. Results: Vascular risk and neurofilament light were not related in the main effect model (p = 0.08). However, interactions emerged for total tau (p = 0.01) and hyperphosphorylated tau (p = 0.002) reflecting vascular risk becoming more associated with cerebrospinal fluid neurofilament light in the context of greater concentrations of tau biomarkers. An interaction also emerged for the Alzheimer's disease biomarker profiles (p = 0.046) where in comparison to the referent 'normal' biomarker group, individuals with abnormal levels of both A beta(42) and total tau showed stronger associations between vascular risk and neurofilament light. Conclusion: Older adults may be more vulnerable to axonal injury in response to higher vascular risk burdens in the context of concomitant Alzheimer's disease pathology.

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