Nicholas M Pajewski1, Fanny M Elahi2, Manjula Kurella Tamura3, Jason D Hinman4, Ilya M Nasrallah5, Joachim H Ix6, Lindsay M Miller6, Lenore J Launer7, Clinton B Wright8, Mark A Supiano9, Alan J Lerner10, Tiffany L Sudduth11, Anthony A Killeen12, Alfred K Cheung13, David M Reboussin1, Donna M Wilcock11, Jeff D Williamson14. 1. Department of Biostatistics and Data Science, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA. 2. Department of Neurology, Memory and Aging Center, Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA. 3. Geriatric Research, Education and Clinical Center, Palo Alto Veterans Affairs Health Care System, California and Division of Nephrology, Stanford University School of Medicine, Palo Alto, California, USA. 4. Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. 5. Department of Radiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 6. Division of Nephrology-Hypertension, University of California San Diego, San Diego, California, USA. 7. Intramural Research Program, National Institute on Aging, Baltimore, Maryland, USA. 8. National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA. 9. Geriatric Research, Education and Clinical Center, Veterans Affairs Salt Lake City Health System, Utah and Division of Geriatrics, University of Utah School of Medicine, Salt Lake City, Utah, USA. 10. Department of Neurology, University Hospitals-Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. 11. Department of Physiology, Sanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA. 12. Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota, USA. 13. Renal Section, Veterans Affairs Salt Lake City Healthcare System, Utah and Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA. 14. Section on Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA.
Abstract
INTRODUCTION: Lowering blood pressure (BP) reduces the risk for cognitive impairment and the progression of cerebral white matter lesions. It is unclear whether hypertension control also influences plasma biomarkers related to Alzheimer's disease and non-disease-specific neurodegeneration. METHODS: We examined the effect of intensive (< 120 mm Hg) versus standard (< 140 mm Hg) BP control on longitudinal changes in plasma amyloid beta (Aβ)40 and Aβ42 , total tau, and neurofilament light chain (NfL) in a subgroup of participants from the Systolic Blood Pressure Intervention Trial (N = 517). RESULTS: Over 3.8 years, there were no significant between-group differences for Aβ40, Aβ42, Aβ42 /Aβ40, or total tau. Intensive treatment was associated with larger increases in NfL compared to standard treatment. Adjusting for kidney function, but not BP, attenuated the association between intensive treatment and NfL. DISCUSSION: Intensive BP treatment was associated with changes in NfL, which were correlated with changes in kidney function associated with intensive treatment. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01206062.
INTRODUCTION: Lowering blood pressure (BP) reduces the risk for cognitive impairment and the progression of cerebral white matter lesions. It is unclear whether hypertension control also influences plasma biomarkers related to Alzheimer's disease and non-disease-specific neurodegeneration. METHODS: We examined the effect of intensive (< 120 mm Hg) versus standard (< 140 mm Hg) BP control on longitudinal changes in plasma amyloid beta (Aβ)40 and Aβ42 , total tau, and neurofilament light chain (NfL) in a subgroup of participants from the Systolic Blood Pressure Intervention Trial (N = 517). RESULTS: Over 3.8 years, there were no significant between-group differences for Aβ40, Aβ42, Aβ42 /Aβ40, or total tau. Intensive treatment was associated with larger increases in NfL compared to standard treatment. Adjusting for kidney function, but not BP, attenuated the association between intensive treatment and NfL. DISCUSSION: Intensive BP treatment was associated with changes in NfL, which were correlated with changes in kidney function associated with intensive treatment. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01206062.
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