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JAMA Neurol. 2014 Oct;71(10):1218-27. doi: 10.1001/jamaneurol.2014.1646.

Midlife hypertension and 20-year cognitive change: the atherosclerosis risk in communities neurocognitive study.

Author information

  • 1Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland2Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
  • 2Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
  • 3Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
  • 4Division of Epidemiology and Community Health, University of Minnesota, Minneapolis.
  • 5Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
  • 6Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina.
  • 7Department of Neurology, Mayo Clinic, Rochester, Minnesota.
  • 8Department of Biostatistics, University of North Carolina at Chapel Hill.
  • 9Department of Medicine, University of Mississippi Medical Center, Jackson.



Hypertension is a treatable potential cause of cognitive decline and dementia, but its greatest influence on cognition may occur in middle age.


To evaluate the association between midlife (48-67 years of age) hypertension and the 20-year change in cognitive performance.


The Atherosclerosis Risk in Communities cohort (1990-1992 through 2011-2013) underwent evaluation at field centers in Washington County, Maryland, Forsyth County, North Carolina, Jackson, Mississippi, and the Minneapolis, Minnesota, suburbs. Of 13 476 African American and white participants with baseline cognitive data, 58.0% of living participants completed the 20-year cognitive follow-up.


Hypertension, prehypertension, or normal blood pressure (BP) at visit 2 (1990-1992) constituted the primary exposure. Systolic BP at visit 2 or 5 (2011-2013) and indication for treatment at visit 2 based on the Eighth Joint National Committee (JNC-8) hypertension guidelines constituted the secondary exposures.


Prespecified outcomes included the 20-year change in scores on the Delayed Word Recall Test, Digit Symbol Substitution Test, and Word Fluency Test and in global cognition.


During 20 years, baseline hypertension was associated with an additional decline of 0.056 global z score points (95% CI, -0.100 to -0.012) and prehypertension was associated nonsignificantly with 0.040 more global z score points of decline (95% CI, -0.085 to 0.005) compared with normal BP. Individuals with hypertension who used antihypertensives had less decline during the 20 years than untreated individuals with hypertension (-0.050 [95% CI, -0.003 to -0.097] vs -0.079 [95% CI, -0.156 to -0.002] global z score points). Having a JNC-8-specified indication for initiating antihypertensive treatment at baseline was associated with a greater 20-year decline (-0.044 [95% CI, -0.085 to -0.003] global z score points) than not having an indication. We observed effect modification by race for the continuous systolic BP analyses (P = .01), with each 20-mm Hg increment at baseline associated with an additional decline of 0.048 (95% CI, -0.074 to -0.022) points in global cognitive z score in whites but not in African Americans (decline, -0.020 [95% CI, -0.026 to 0.066] points). Systolic BP at the end of follow-up was not associated with the preceding 20 years of cognitive change in either group. Methods to account for bias owing to attrition strengthened the magnitude of some associations.


Midlife hypertension and elevated midlife but not late-life systolic BP was associated with more cognitive decline during the 20 years of the study. Greater decline is found with higher midlife BP in whites than in African Americans.

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