Link Between Cardiovascular-Risk Management And Dementia Protection Remains Elusive

Intensive blood pressure control did not lead to any consistent or clinically meaningful differences in MRI imaging biomarkers of Alzheimer's disease (AD)-related neurodegeneration in a substudy of the SPRINT MIND trial.

Furthermore, compared with standard BP control, intensive BP control was associated with larger decreases in hippocampal volume, Dr. Ilya Nasrallah of the Hospital of the University of Pennsylvania, in Philadelphia, and colleagues report in JAMA Neurology.

"The findings of the SPRINT study overall suggest that the primary benefit of intensive hypertension control is in reducing cardiovascular events. But the SPRINT MIND data thus far do not point to a clear additional benefit of such treatment in maintaining cognitive function or reducing the risk of AD," write the authors of an accompanying editorial.

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Earlier studies had suggested that better BP control could reduce the risk of cognitive impairment and dementia, but it is unclear if and how much AD pathology is affected by hypertension control, according to the researchers.

To investigate, they evaluated MRI brain scans obtained at baseline and four years later in 454 participants from SPRINT MIND; 251 had been randomized to intensive BP control (systolic BP < 120 mm Hg) and 203 to standard BP control (systolic < 140 mm Hg). At baseline, participants had a mean age of 67 years, 40% were women and 32% were Black.

While amyloid and tau biomarkers were not available in this study, the investigators evaluated a variety of MRI measurements optimized for detection of AD-sensitive neurodegeneration and white-matter-tract changes, they explain.

Yet, they found no evidence of a treatment group difference for any of the other markers of AD-related neurodegeneration, including AD regional atrophy, cerebral blood flow or mean fractional anisotropy.

Meanwhile, mean hippocampal volume decreased from 7.45 to 7.39 cm3 in patients receiving intensive treatment, compared with a decrease from 7.48 to 7.46 cm3 in the control group (P=0.3).

This result is "challenging to interpret," Dr. Nasrallaha and colleagues admit. They say the lack of treatment group differences for the other measured AD-related biomarkers "would seem to suggest that the hippocampal volume result does not likely reflect differential development of AD-related neurodegeneration."

"However, it remains possible that the hippocampal volume result is due to a difference in early AD that is not detected by the other biomarkers. Alternatively, it could be a manifestation of the global effect of intensive treatment on TBV, related to volume status or another pathology," they suggest.

In their editorial, Dr. Susan Landau and Dr. Theresa Harrison of the Helen Wills Neuroscience Institute, University of California, Berkeley, make the point that, while counterintuitive, increased hippocampal atrophy is "consistent with a recent report in the same SPRINT MIND sample of an intensive intervention-related association with another non-AD specific biomarker: decreased total brain volume."

The absence of amyloid and tau measurements in the current analysis "limits definitive conclusions about the specificity of these findings to AD. However, the MRI results and the lack of an influence of intensive treatment on AD incidence in the main trial together do not support a role for hypertension control in mitigating AD risk," Dr. Landau and Dr. Harrison say.

At present, a link between cardiovascular risk management and AD "is still elusive. Future work is needed to understand how AD and cerebrovascular pathophysiology contribute to the complex relationship between cardiovascular health and cognitive decline," they conclude.

—Reuters Staff

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