Among older adults ≥74 years of age, greater aortic stiffening is associated with biomarker evidence of neuroinflammation, tau phosphorylation, synaptic dysfunction, and neurodegeneration (P<0.001).
Observational
Alzheimer disease pathology
Aortic stiffness (Pulse wave velocity)
CSF evidence of core Alzheimer disease pathology, neurodegeneration, synaptic dysfunction, neuroaxonal injury, and neuroinflammation, p=< 0.001
p-value: p=< 0.001
OBJECTIVES: To test the hypothesis that increased aortic stiffening is associated with greater CSF evidence of core Alzheimer disease pathology (β-amyloid Aβ, phosphorylated tau p-tau), neurodegeneration (total tau t-tau), synaptic dysfunction (neurogranin), neuroaxonal injury (neurofilament light NFL), and neuroinflammation (YKL-40, soluble triggering receptor expressed on myeloid cells 2 sTREM2), we analyzed pulse wave velocity (PWV) data and CSF data among older adults. METHODS: ε4, and hypertension on each biomarker. RESULTS: < 0.001). CONCLUSIONS: Among our oldest participants, ≥74 years of age, greater aortic stiffening is associated with in vivo biomarker evidence of neuroinflammation, tau phosphorylation, synaptic dysfunction, and neurodegeneration, but not amyloidosis. Central arterial stiffening may lead to cumulative cerebral microcirculatory damage and reduced blood flow delivery to tissue, resulting in neuroinflammation and neurodegeneration in more advanced age.
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Elizabeth E. Moore
Mass General Brigham
Dandan Liu
University of Nebraska–Lincoln
Judy Li
Rutgers, The State University of New Jersey
Neurology
University College London
University of Gothenburg
National Hospital for Neurology and Neurosurgery
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Moore et al. (Mon,) conducted a observational in Alzheimer disease pathology. Aortic stiffness (Pulse wave velocity) was evaluated on CSF evidence of core Alzheimer disease pathology, neurodegeneration, synaptic dysfunction, neuroaxonal injury, and neuroinflammation (p=< 0.001). Among older adults ≥74 years of age, greater aortic stiffening is associated with biomarker evidence of neuroinflammation, tau phosphorylation, synaptic dysfunction, and neurodegeneration (P<0.001).
synapsesocial.com/papers/6a07b5d915d371b388386c61 — DOI: https://doi.org/10.1212/wnl.0000000000012257
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