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The effect of parasympathetic central autonomic network (CAN) impairment on this relationship has not been assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Determine whether parasympathetic CAN network function affects the relationship between BPV and neurodegenerative markers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>100 independently living older adults (55\u201389 years) underwent continuous blood pressure monitoring, neuropsychological testing, venipuncture, and brain MRI. Hippocampal volumes and entorhinal cortex thicknesses were assessed. Functional connectivity within a parasympathetic cardiovascular control network was used as a measure of parasympathetic CAN function. Plasma glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) were used as measures of glial and neuronal injury, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Elevated BPV was associated with left hippocampal atrophy (p\u2009\n                      <jats:italic toggle=\"yes\">=<\/jats:italic>\n                      \u20090.03) and elevated plasma GFAP (p\u2009\n                      <jats:italic toggle=\"yes\">=<\/jats:italic>\n                      \u20090.005) independent of age, sex, vascular risk factor burden, total intracranial volume (when applicable) and average blood pressure. These relationships were not mediated by parasympathetic central autonomic network impairment. Instead, parasympathetic CAN impairment conferred a vulnerability to elevated BPV. In participants with decreased parasympathetic CAN connectivity elevated BPV was associated with left entorhinal cortex atrophy (p\u2009\n                      <jats:italic toggle=\"yes\">=<\/jats:italic>\n                      \u20090.0001), elevated plasma GFAP (p\u2009\n                      <jats:italic toggle=\"yes\">=<\/jats:italic>\n                      \u20090.0001), elevated plasma NfL (p\u2009\n                      <jats:italic toggle=\"yes\">=<\/jats:italic>\n                      \u20090.001), and memory impairment (p\u2009\n                      <jats:italic toggle=\"yes\">=<\/jats:italic>\n                      \u20090.007).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Findings suggest elevated beat-to-beat BPV is directly related to brain injury, and this effect is not mediated by CAN dysfunction. Instead, CAN impairment may confer a susceptibility to glial and neuronal injury in older adults with elevated beat-to-beat blood pressure variability. Mechanisms underlying increased susceptibility to BPV elevation in those with CAN dysfunction warrants further study.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877251376715","type":"journal-article","created":{"date-parts":[[2025,9,15]],"date-time":"2025-09-15T17:50:14Z","timestamp":1757958614000},"page":"411-420","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Impaired parasympathetic network function confers susceptibility to neurodegeneration and memory impairment in older adults with elevated beat-to-beat blood pressure variability"],"prefix":"10.1177","volume":"108","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9634-702X","authenticated-orcid":false,"given":"Trevor","family":"Lohman","sequence":"first","affiliation":[{"name":"Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, USA"},{"name":"Keck School of Medicine, University of 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