In a new study, researchers found high blood pressure and large increases in blood pressure in midlife may be associated with brain pathologies in later life.
They found that high blood pressure and rising blood pressure between ages 36-53 were linked to smaller brain volume, white matter lesions in later years.
But high blood pressure is not linked to reduced cognition or the build-up of beta-amyloid plaques—one of the key proteins associated with Alzheimer’s disease.
High blood pressure is known to increase the risk for cognitive impairment later in life, but exactly how and when it increases risk is unclear.
The study examined 502 people who have been tracked since their birth in 1946. They were cognitively healthy.
All participants had had blood pressure taken at 36, 43, 53, 60-64, and 69 years old.
The researchers measured each participant’s overall brain volume at about 70 years of age, along with the volume of the hippocampus, the extent of white matter brain lesions, amount of beta-amyloid plaques, and cognitive capabilities.
They found that high blood pressure (140/90 mm Hg or higher) may lead to reductions in brain volume and higher levels of white matter hyperintensities within the brain (white matter brain lesions).
Higher and rising blood pressure between the ages of 36 and 53 had the strongest associations with smaller brain volume and increases in white matter brain lesions in later life.
The findings suggest that blood pressure monitoring and interventions may need to start at, or before, 40 years to maximize later brain health.
The research builds on existing evidence around the role of blood pressure and subsequent brain pathology.
The team also found no evidence that blood pressure affected cognition or the build-up of beta-amyloid plaques.
This suggests that links between midlife blood pressure and late-life brain health are unlikely to be occurring through the build-up of beta-amyloid, which is thought to be one of the earliest changes seen in Alzheimer’s disease.
The lead author of the study is Professor Jonathan M Schott, University College London, UK.
The study is published in The Lancet Neurology.
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